ETHMOID ΣΤΗμοιΔ ΕΘμοιΔ ΗΘμοιχξ ἡθμόις,

 

The ethmoid bone (/ˈɛθmɔɪd/;^[1][2] from Ancient Greek: ἡθμός, romanized: hēthmós, lit. 'sieve') is an unpaired bone in the skull that separates the nasal cavity from the brain. It is located at the roof of the nose, between the two orbits. The cubical bone is lightweight due to a spongy construction. The ethmoid bone is one of the bones that make up the orbit of the eye.

Structure

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The ethmoid bone is an anterior cranial bone located between the eyes.^[3] It contributes to the medial wall of the orbit, the nasal cavity, and the nasal septum.^[3] The ethmoid has three parts: cribriform plate, ethmoidal labyrinth, and perpendicular plate. The cribriform plate forms the roof of the nasal cavity and also contributes to formation of the anterior cranial fossa,^[4] the ethmoidal labyrinth consists of a large mass on either side of the perpendicular plate, and the perpendicular plate forms the superior two-thirds of the nasal septum.^[3] Between the orbital plate and the nasal conchae are the ethmoidal sinuses or ethmoidal air cells, which are a variable number of small cavities in the lateral mass of the ethmoid.^[5][6]

By Images are generated by Life Science Databases(LSDB), animated by was a bee. - from Anatomography[3] website maintained by Life Science Databases(LSDB).You can get images that compose this animation through this URL[4].次のアドレスからこの動画の作成に使用した元画像を取得できます[5]。, CC BY-SA 2.1 jp, https://commons.wikimedia.org/w/index.php?curid=7737685

The ethmoid articulates with thirteen bones:

• two bones of the neurocranium—the frontal, and the sphenoid (at the sphenoidal body and at the sphenoidal conchae).
• eleven bones of the viscerocranium—, two nasal bones, two maxillae, two lacrimals, two palatines, two inferior nasal conchae, and the vomer.

Development

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The ethmoid is ossified in the cartilage of the nasal capsule by three centers: one for the perpendicular plate, and one for each labyrinth.

The labyrinths are first developed, ossific granules making their appearance in the region of the lamina papyracea between the fourth and fifth months of fetal life, and extending into the conchæ.

At birth, the bone consists of the two labyrinths, which are small and ill-developed. During the first year after birth, the perpendicular plate and crista galli begin to ossify from a single center, and are joined to the labyrinths about the beginning of the second year.

The cribriform plate is ossified partly from the perpendicular plate and partly from the labyrinths.

The development of the ethmoidal cells begins during fetal life.

Magnetoreception is a sense which allows an organism to detect the Earth's magnetic field. Animals with this sense include some arthropods, molluscs, and vertebrates (fish, amphibians, reptiles, birds, and mammals). The sense is mainly used for orientation and navigation, but it may help some animals to form regional maps. Experiments on migratory birds provide evidence that they make use of a cryptochrome protein in the eye, relying on the quantum radical pair mechanism to perceive magnetic fields. This effect is extremely sensitive to weak magnetic fields, and readily disturbed by radio-frequency interference, unlike a conventional iron compass.

Birds have iron-containing materials in their upper beaks. There is some evidence that this provides a magnetic sense, mediated by the trigeminal nerve, but the mechanism is unknown.

Cartilaginous fish including sharks and stingrays can detect small variations in electric potential with their electroreceptive organs, the ampullae of Lorenzini. These appear to be able to detect magnetic fields by induction. There is some evidence that these fish use magnetic fields in navigation.

Bioelectromagnetism is studied primarily through the techniques of electrophysiology. In the late eighteenth century, the Italian physician and physicist Luigi Galvani first recorded the phenomenon while dissecting a frog at a table where he had been conducting experiments with static electricity. Galvani coined the term animal electricity to describe the phenomenon, while contemporaries labeled it galvanism. Galvani and contemporaries regarded muscle activation as resulting from an electrical fluid or substance in the nerves.^[1] Short-lived electrical events called action potentials occur in several types of animal cells which are called excitable cells, a category of cell include neurons, muscle cells, and endocrine cells, as well as in some plant cells. These action potentials are used to facilitate inter-cellular communication and activate intracellular processes. The physiological phenomena of action potentials are possible because voltage-gated ion channels allow the resting potential caused by electrochemical gradient on either side of a cell membrane to resolve.^{[citation needed]}.

Several animals are suspected to have the ability to sense electromagnetic fields; for example, several aquatic animals have structures potentially capable of sensing changes in voltage caused by a changing magnetic field,^[2] while migratory birds are thought to use magnetoreception in navigation.^[3][4][5]

Pigeons and other migratory birds are thought to use a sense of the Earth's magnetic field in navigation.^[6][7][8][9]

Bioeffects of electromagnetic radiation

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Most of the molecules in the human body interact weakly with electromagnetic fields in the radio frequency or extremely low frequency bands.^{[citation needed]} One such interaction is absorption of energy from the fields, which can cause tissue to heat up; more intense fields will produce greater heating. This can lead to biological effects ranging from muscle relaxation (as produced by a diathermy device) to burns.^[10] Many nations and regulatory bodies like the International Commission on Non-Ionizing Radiation Protection have established safety guidelines to limit EMF exposure to a non-thermal level. This can be defined as either heating only to the point where the excess heat can be dissipated, or as a fixed increase in temperature not detectable with current instruments like 0.1 °C.^{[citation needed]} However, biological effects have been shown to be present for these non-thermal exposures;^{[citation needed]} Various mechanisms have been proposed to explain these,^[11] and there may be several mechanisms underlying the differing phenomena observed.

The idea that high-frequency electromagnetic currents could have therapeutic effects was explored independently around the same time (1890–1891) by French physician and biophysicist Jacques Arsene d'Arsonval and Serbian American engineer Nikola Tesla.^[1][2][3] d'Arsonval had been studying medical applications for electricity in the 1880s and performed the first systematic studies in 1890 of the effect of alternating current on the body, and discovered that frequencies above 10 kHz did not cause the physiological reaction of electric shock, but warming.^[2][3][7][8] He also developed the three methods that have been used to apply high-frequency current to the body: contact electrodes, capacitive plates, and inductive coils.^[3] Nikola Tesla first noted around 1891 the ability of high-frequency currents to produce heat in the body and suggested its use in medicine.^[1]

By 1900 application of high-frequency current to the body was used experimentally to treat a wide variety of medical conditions in the new medical field of electrotherapy. In 1899 Austrian chemist von Zaynek determined the rate of heat production in tissue as a function of frequency and current density, and first proposed using high-frequency currents for deep heating therapy.^[2] In 1908 German physician Karl Franz Nagelschmidt coined the term diathermy, and performed the first extensive experiments on patients.^[3] Nagelschmidt is considered the founder of the field. He wrote the first textbook on diathermy in 1913, which revolutionized the field.^[2][3]

Until the 1920s noisy spark-discharge Tesla coil and Oudin coil machines were used. These were limited to frequencies of 0.1–2 MHz, called "longwave" diathermy. The current was applied directly to the body with contact electrodes, which could cause skin burns. In the 1920s the development of vacuum tube machines allowed frequencies to be increased to 10–300 MHz, called "shortwave" diathermy. The energy was applied to the body with inductive coils of wire or capacitive plates insulated from the body, which reduced the risk of burns. By the 1940s microwaves were being used experimentally.

Electrotherapy is the use of electrical energy as a medical treatment.^[1] In medicine, the term electrotherapy can apply to a variety of treatments, including the use of electrical devices such as deep brain stimulators for neurological disease. The term has also been applied specifically to the use of electric current to speed wound healing. The use of EMS is also very wide for managing muscular pain.

An Oudin coil, also called an Oudin oscillator or Oudin resonator, is a resonant transformer circuit that generates very high voltage, high frequency alternating current (AC) electricity at low current levels,^[1][2][3] used in the obsolete forms of electrotherapy around the turn of the 20th century.^[4] It is very similar to the Tesla coil, with the difference being that the Oudin coil was connected as an autotransformer.^[2][5] It was invented in 1893 by French physician Paul Marie Oudin^[6] as a modification of physician Jacques Arsene d'Arsonval's electrotherapy equipment^[7][8] and used in medical diathermy therapy as well as quack medicine until perhaps 1940. The high voltage output terminal of the coil was connected to an insulated handheld electrode which produced luminous brush discharges, which were applied to the patient's body to treat various medical conditions in electrotherapy.^[4]

How it works

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Oudin and Tesla coils are spark-excited air-core double-tuned transformer circuits that use resonance to generate very high voltages at low currents.^[9][10] They produce alternating current in the radio frequency (RF) range. The medical coils of the early 20th century produced potentials of 50,000 up to a million volts, at frequencies in the range 200 kHz to 5 MHz.^[4] The primary circuit of the coil has Leyden jar capacitors (C) which in combination with the primary winding of the coil (L1) make a resonant circuit (tuned circuit).^[4] In medical coils usually two capacitors were used for safety, one in each side of the primary circuit, to isolate the patient completely from the potentially lethal low frequency primary current. The primary circuit also has a spark gap (SG) that acts as a switch to excite oscillations in the primary. The primary circuit is powered by a high voltage transformer or induction coil^[4] (T) at a potential of 2 - 15 kV. The transformer repeatedly charges the capacitors, which then discharge through the spark gap and the primary winding (a detailed description of the operation cycle in the Tesla coil article also applies to the Oudin coil). This cycle is repeated many times per second. During each spark, the charge moves rapidly back and forth between the capacitor plates through the primary coil, creating a damped RF oscillating current in the primary tuned circuit which induced the high voltage in the secondary.

The secondary winding (L2) is open-circuited, and connected to the output electrode of the device. In the Oudin coil, one side of the primary winding (L1) is grounded and the other side is connected to the secondary, so the primary and secondary are in series. There were two versions of the Oudin coil:^[3][11][12]

Early type Oudin coil, around 1904, with separate primary and secondary coils. In the drawing the primary (L1) is the small horizontal coil visible between the Leyden jars and the large vertical secondary resonator coil. The transformer (T) which powers the circuit is not shown.

• In earlier Oudin circuits the two coils were separate, not magnetically coupled, with a small horizontal primary "D'Arsonval" coil (L1) of 20-40 turns with a tap connected to a large vertical secondary "Oudin resonator" (L2) with many turns of fine wire (400 - 600 in large coils, 100 - 300 in small ones),^[2] connected to the high voltage terminal on top. In this circuit the high voltage was generated entirely by self-resonance in the high Q secondary coil. The addition of the "resonator" coil to the "D'Arsonval" coil was Oudin's contribution; the rest of the circuit was invented by Jacques D'Arsonval.^[3]

Later type with primary and secondary wound on the same form to make an autotransformer. The primary is the coarse winding at the bottom. In both pictures the spark gap (SG) is enclosed in a small box (S) at right to reduce noise.

• In later Oudin circuits the coils were magnetically coupled, forming an autotransformer, so the primary induces an EMF in the secondary by electromagnetic induction. Both coils were usually wound on the same coil form, the primary consisting of relatively few turns of heavy wire at the bottom with an adjustable tap, connected to the secondary winding, made of many turns of fine wire.^[3] Oudin found this circuit produced higher voltages due to the large turns ratio of the transformer.

Although it doesn't include a capacitor, the secondary winding is also a resonant circuit (electrical resonator); the parasitic capacitance between the ends of the secondary coil resonates with the large inductance of the secondary at a particular resonant frequency. When it is excited at this frequency by the primary, large oscillating voltages are induced in the secondary. The number of turns in the primary winding, and thus the resonant frequency of the primary, could be adjusted with a tap on the coil. When the two tuned circuits are adjusted to resonate at the same frequency, the large turns ratio of the coil, aided by the high Q of the tuned circuits, steps up the primary voltage to hundreds of thousands to millions of volts at the secondary.

The secondary is directly connected to the primary circuit, which carries lethal low frequency 50/60 Hz currents at thousands of volts from the power transformer. Since the Oudin coil was a medical device, with the secondary current applied directly to a person's body, for safety the Oudin circuit has two capacitors (C), one in each leg of the primary, to completely isolate the coil and output electrode from the supply transformer at the mains frequency.^[13] Because two identical capacitors in series have half the capacitance of a single capacitor, the resonant frequency of the Oudin circuit is

${\displaystyle f=\frac{1}{2\pi \sqrt{L_{1}C/2}}}$

An action potential occurs when the membrane potential of a specific cell rapidly rises and falls.^[1] This depolarization then causes adjacent locations to similarly depolarize. Action potentials occur in several types of excitable cells, which include animal cells like neurons and muscle cells, as well as some plant cells. Certain endocrine cells such as pancreatic beta cells, and certain cells of the anterior pituitary gland are also excitable cells.^[2]

In neurons, action potentials play a central role in cell–cell communication by providing for—or with regard to saltatory conduction, assisting—the propagation of signals along the neuron's axon toward synaptic boutons situated at the ends of an axon; these signals can then connect with other neurons at synapses, or to motor cells or glands. In other types of cells, their main function is to activate intracellular processes. In muscle cells, for example, an action potential is the first step in the chain of events leading to contraction. In beta cells of the pancreas, they provoke release of insulin.^[a] Action potentials in neurons are also known as "nerve impulses" or "spikes", and the temporal sequence of action potentials generated by a neuron is called its "spike train". A neuron that emits an action potential, or nerve impulse, is often said to "fire".

Action potentials are generated by special types of voltage-gated ion channels embedded in a cell's plasma membrane.^[b] These channels are shut when the membrane potential is near the (negative) resting potential of the cell, but they rapidly begin to open if the membrane potential increases to a precisely defined threshold voltage, depolarising the transmembrane potential.^[b] When the channels open, they allow an inward flow of sodium ions, which changes the electrochemical gradient, which in turn produces a further rise in the membrane potential towards zero. This then causes more channels to open, producing a greater electric current across the cell membrane and so on. The process proceeds explosively until all of the available ion channels are open, resulting in a large upswing in the membrane potential. The rapid influx of sodium ions causes the polarity of the plasma membrane to reverse, and the ion channels then rapidly inactivate. As the sodium channels close, sodium ions can no longer enter the neuron, and they are then actively transported back out of the plasma membrane. Potassium channels are then activated, and there is an outward current of potassium ions, returning the electrochemical gradient to the resting state. After an action potential has occurred, there is a transient negative shift, called the afterhyperpolarization.

Membrane potential (also transmembrane potential or membrane voltage) is the difference in electric potential between the interior and the exterior of a biological cell. It equals the interior potential minus the exterior potential. This is the energy (i.e. work) per charge which is required to move a (very small) positive charge at constant velocity across the cell membrane from the exterior to the interior. (If the charge is allowed to change velocity, the change of kinetic energy and production of radiation must be taken into account.)

Typical values of membrane potential, normally given in units of milli volts and denoted as mV, range from –80 mV to –40 mV. For such typical negative membrane potentials, positive work is required to move a positive charge from the interior to the exterior. However, thermal kinetic energy allows ions to overcome the potential difference. For a selectively permeable membrane, this permits a net flow against the gradient. This is a kind of osmosis.

Ion concentration gradients

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Key: Blue pentagons – sodium ions; Purple squares – potassium ions; Yellow circles – chloride ions; Orange rectangles – membrane-impermeable anions (these arise from a variety of sources including proteins).
The large purple structure with an arrow represents a transmembrane potassium channel and the direction of net potassium movement.

Differences in the concentrations of ions on opposite sides of a cellular membrane lead to a voltage called the membrane potential.^[3]

Many ions have a concentration gradient across the membrane, including potassium (K⁺), which is at a high concentration inside and a low concentration outside the membrane. Sodium (Na⁺) and chloride (Cl⁻) ions are at high concentrations in the extracellular region, and low concentrations in the intracellular regions. These concentration gradients provide the potential energy to drive the formation of the membrane potential. This voltage is established when the membrane has permeability to one or more ions.

In the simplest case, illustrated here, if the membrane is selectively permeable to potassium, these positively charged ions can diffuse down the concentration gradient to the outside of the cell, leaving behind uncompensated negative charges. This separation of charges is what causes the membrane potential.

The system as a whole is electro-neutral. The uncompensated positive charges outside the cell, and the uncompensated negative charges inside the cell, physically line up on the membrane surface and attract each other across the lipid bilayer. Thus, the membrane potential is physically located only in the immediate vicinity of the membrane. It is the separation of these charges across the membrane that is the basis of the membrane voltage.

This diagram is only an approximation of the ionic contributions to the membrane potential. Other ions including sodium, chloride, calcium, and others play a more minor role, even though they have strong concentration gradients, because they have more limited permeability than potassium.

Physical basis

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The membrane potential in a cell derives ultimately from two factors: electrical force and diffusion. Electrical force arises from the mutual attraction between particles with opposite electrical charges (positive and negative) and the mutual repulsion between particles with the same type of charge (both positive or both negative). Diffusion arises from the statistical tendency of particles to redistribute from regions where they are highly concentrated to regions where the concentration is low.

Voltage

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Main article: Voltage

Electric field (arrows) and contours of constant voltage created by a pair of oppositely charged objects. The electric field is at right angles to the voltage contours, and the field is strongest where the spacing between contours is the smallest.

Voltage, which is synonymous with difference in electrical potential, is the ability to drive an electric current across a resistance. Indeed, the simplest definition of a voltage is given by Ohm's law: V=IR, where V is voltage, I is current and R is resistance. If a voltage source such as a battery is placed in an electrical circuit, the higher the voltage of the source the greater the amount of current that it will drive across the available resistance. The functional significance of voltage lies only in potential differences between two points in a circuit. The idea of a voltage at a single point is meaningless. It is conventional in electronics to assign a voltage of zero to some arbitrarily chosen element of the circuit, and then assign voltages for other elements measured relative to that zero point. There is no significance in which element is chosen as the zero point—the function of a circuit depends only on the differences not on voltages per se. However, in most cases and by convention, the zero level is most often assigned to the portion of a circuit that is in contact with ground.

The same principle applies to voltage in cell biology. In electrically active tissue, the potential difference between any two points can be measured by inserting an electrode at each point, for example one inside and one outside the cell, and connecting both electrodes to the leads of what is in essence a specialized voltmeter. By convention, the zero potential value is assigned to the outside of the cell and the sign of the potential difference between the outside and the inside is determined by the potential of the inside relative to the outside zero.

In mathematical terms, the definition of voltage begins with the concept of an electric field E, a vector field assigning a magnitude and direction to each point in space. In many situations, the electric field is a conservative field, which means that it can be expressed as the gradient of a scalar function V, that is, E = –∇V. This scalar field V is referred to as the voltage distribution. The definition allows for an arbitrary constant of integration—this is why absolute values of voltage are not meaningful. In general, electric fields can be treated as conservative only if magnetic fields do not significantly influence them, but this condition usually applies well to biological tissue.

Because the electric field is the gradient of the voltage distribution, rapid changes in voltage within a small region imply a strong electric field; on the converse, if the voltage remains approximately the same over a large region, the electric fields in that region must be weak. A strong electric field, equivalent to a strong voltage gradient, implies that a strong force is exerted on any charged particles that lie within the region.

Ions and the forces driving their motion

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Main articles: Ion, Diffusion, Electrochemical gradient, and Electrophoretic mobility

Ions (pink circles) will flow across a membrane from the higher concentration to the lower concentration (down a concentration gradient), causing a current. However, this creates a voltage across the membrane that opposes the ions' motion. When this voltage reaches the equilibrium value, the two balance and the flow of ions stops.^[4]

Electrical signals within biological organisms are, in general, driven by ions.^[5]

An ion (/ˈaɪ.ɒn, -ən/)^[1] is an atom or molecule with a net electrical charge. The charge of an electron is considered to be negative by convention and this charge is equal and opposite to the charge of a proton, which is considered to be positive by convention. The net charge of an ion is not zero because its total number of electrons is unequal to its total number of protons.

   

A cation is a positively charged ion with fewer electrons than protons^[2] (e.g. K⁺ (potassium ion)) while an anion is a negatively charged ion with more electrons than protons.^[3] (e.g. Cl^- (chloride ion) and OH^- (hydroxide ion)). Opposite electric charges are pulled towards one another by electrostatic force, so cations and anions attract each other and readily form ionic compounds.

 The most important cations for the action potential are sodium (Na⁺) and potassium (K⁺).^[6] Both of these are monovalent cations that carry a single positive charge. Action potentials can also involve calcium (Ca²⁺),^[7] which is a divalent cation that carries a double positive charge. The chloride anion (Cl⁻) plays a major role in the action potentials of some algae,^[8] but plays a negligible role in the action potentials of most animals.^[9]

Ions cross the cell membrane under two influences: diffusion and electric fields. A simple example wherein two solutions—A and B—are separated by a porous barrier illustrates that diffusion will ensure that they will eventually mix into equal solutions. This mixing occurs because of the difference in their concentrations. The region with high concentration will diffuse out toward the region with low concentration. To extend the example, let solution A have 30 sodium ions and 30 chloride ions. Also, let solution B have only 20 sodium ions and 20 chloride ions. Assuming the barrier allows both types of ions to travel through it, then a steady state will be reached whereby both solutions have 25 sodium ions and 25 chloride ions. If, however, the porous barrier is selective to which ions are let through, then diffusion alone will not determine the resulting solution. Returning to the previous example, let's now construct a barrier that is permeable only to sodium ions. Now, only sodium is allowed to diffuse cross the barrier from its higher concentration in solution A to the lower concentration in solution B. This will result in a greater accumulation of sodium ions than chloride ions in solution B and a lesser number of sodium ions than chloride ions in solution A.

This means that there is a net positive charge in solution B from the higher concentration of positively charged sodium ions than negatively charged chloride ions. Likewise, there is a net negative charge in solution A from the greater concentration of negative chloride ions than positive sodium ions. Since opposite charges attract and like charges repel, the ions are now also influenced by electrical fields as well as forces of diffusion. Therefore, positive sodium ions will be less likely to travel to the now-more-positive B solution and remain in the now-more-negative A solution. The point at which the forces of the electric fields completely counteract the force due to diffusion is called the equilibrium potential. At this point, the net flow of the specific ion (in this case sodium) is zero.

An electrochemical gradient is a gradient of electrochemical potential, usually for an ion that can move across a membrane. The gradient consists of two parts:

• The chemical gradient, or difference in solute concentration across a membrane.
• The electrical gradient, or difference in charge across a membrane.

When there are unequal concentrations of an ion across a permeable membrane, the ion will move across the membrane from the area of higher concentration to the area of lower concentration through simple diffusion. Ions also carry an electric charge that forms an electric potential across a membrane. If there is an unequal distribution of charges across the membrane, then the difference in electric potential generates a force that drives ion diffusion until the charges are balanced on both sides of the membrane.

Electrochemical gradients are essential to the operation of batteries and other electrochemical cells, photosynthesis and cellular respiration, and certain other biological processes.

Plasma membranes

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The cell membrane, also called the plasma membrane or plasmalemma, is a semipermeable lipid bilayer common to all living cells. It contains a variety of biological molecules, primarily proteins and lipids, which are involved in a vast array of cellular processes.

Every cell is enclosed in a plasma membrane, which has the structure of a lipid bilayer with many types of large molecules embedded in it. Because it is made of lipid molecules, the plasma membrane intrinsically has a high electrical resistivity, in other words a low intrinsic permeability to ions. However, some of the molecules embedded in the membrane are capable either of actively transporting ions from one side of the membrane to the other or of providing channels through which they can move.^[10]

In electrical terminology, the plasma membrane functions as a combined resistor and capacitor. Resistance arises from the fact that the membrane impedes the movement of charges across it. Capacitance arises from the fact that the lipid bilayer is so thin that an accumulation of charged particles on one side gives rise to an electrical force that pulls oppositely charged particles toward the other side. The capacitance of the membrane is relatively unaffected by the molecules that are embedded in it, so it has a more or less invariant value estimated at 2 μF/cm² (the total capacitance of a patch of membrane is proportional to its area). The conductance of a pure lipid bilayer is so low, on the other hand, that in biological situations it is always dominated by the conductance of alternative pathways provided by embedded molecules. Thus, the capacitance of the membrane is more or less fixed, but the resistance is highly variable.

The thickness of a plasma membrane is estimated to be about 7-8 nanometers. Because the membrane is so thin, it does not take a very large transmembrane voltage to create a strong electric field within it. Typical membrane potentials in animal cells are on the order of 100 millivolts (that is, one tenth of a volt), but calculations show that this generates an electric field close to the maximum that the membrane can sustain—it has been calculated that a voltage difference much larger than 200 millivolts could cause dielectric breakdown, that is, arcing across the membrane.

Facilitated diffusion and transport

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Facilitated diffusion in cell membranes, showing ion channels and carrier proteins

The resistance of a pure lipid bilayer to the passage of ions across it is very high, but structures embedded in the membrane can greatly enhance ion movement, either actively or passively, via mechanisms called facilitated transport and facilitated diffusion. The two types of structure that play the largest roles are ion channels and ion pumps, both usually formed from assemblages of protein molecules. Ion channels provide passageways through which ions can move. In most cases, an ion channel is permeable only to specific types of ions (for example, sodium and potassium but not chloride or calcium), and sometimes the permeability varies depending on the direction of ion movement. Ion pumps, also known as ion transporters or carrier proteins, actively transport specific types of ions from one side of the membrane to the other, sometimes using energy derived from metabolic processes to do so.

Ion pumps

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The sodium-potassium pump uses energy derived from ATP to exchange sodium for potassium ions across the membrane.

Main articles: Ion transporter and Active transport

Ion pumps are integral membrane proteins that carry out active transport, i.e., use cellular energy (ATP) to "pump" the ions against their concentration gradient.^[11] Such ion pumps take in ions from one side of the membrane (decreasing its concentration there) and release them on the other side (increasing its concentration there).

The ion pump most relevant to the action potential is the sodium–potassium pump, which transports three sodium ions out of the cell and two potassium ions in.^[12][13] As a consequence, the concentration of potassium ions K⁺ inside the neuron is roughly 30-fold larger than the outside concentration, whereas the sodium concentration outside is roughly five-fold larger than inside.^[13][14][15] In a similar manner, other ions have different concentrations inside and outside the neuron, such as calcium, chloride and magnesium.^[15]

If the numbers of each type of ion were equal, the sodium–potassium pump would be electrically neutral, but, because of the three-for-two exchange, it gives a net movement of one positive charge from intracellular to extracellular for each cycle, thereby contributing to a positive voltage difference. The pump has three effects: (1) it makes the sodium concentration high in the extracellular space and low in the intracellular space; (2) it makes the potassium concentration high in the intracellular space and low in the extracellular space; (3) it gives the intracellular space a negative voltage with respect to the extracellular space.

The sodium-potassium pump is relatively slow in operation. If a cell were initialized with equal concentrations of sodium and potassium everywhere, it would take hours for the pump to establish equilibrium. The pump operates constantly, but becomes progressively less efficient as the concentrations of sodium and potassium available for pumping are reduced.

Ion pumps influence the action potential only by establishing the relative ratio of intracellular and extracellular ion concentrations. The action potential involves mainly the opening and closing of ion channels not ion pumps. If the ion pumps are turned off by removing their energy source, or by adding an inhibitor such as ouabain, the axon can still fire hundreds of thousands of action potentials before their amplitudes begin to decay significantly.^[11] In particular, ion pumps play no significant role in the repolarization of the membrane after an action potential.^[6]

Another functionally important ion pump is the sodium-calcium exchanger. This pump operates in a conceptually similar way to the sodium-potassium pump, except that in each cycle it exchanges three Na⁺ from the extracellular space for one Ca⁺⁺ from the intracellular space. Because the net flow of charge is inward, this pump runs "downhill", in effect, and therefore does not require any energy source except the membrane voltage. Its most important effect is to pump calcium outward—it also allows an inward flow of sodium, thereby counteracting the sodium-potassium pump, but, because overall sodium and potassium concentrations are much higher than calcium concentrations, this effect is relatively unimportant. The net result of the sodium-calcium exchanger is that in the resting state, intracellular calcium concentrations become very low.

Ion channels

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Main articles: Ion channel and Passive transport

Despite the small differences in their radii,^[16] ions rarely go through the "wrong" channel. For example, sodium or calcium ions rarely pass through a potassium channel.

Ion channels are integral membrane proteins with a pore through which ions can travel between extracellular space and cell interior. Most channels are specific (selective) for one ion; for example, most potassium channels are characterized by 1000:1 selectivity ratio for potassium over sodium, though potassium and sodium ions have the same charge and differ only slightly in their radius. The channel pore is typically so small that ions must pass through it in single-file order.^[17] Channel pores can be either open or closed for ion passage, although a number of channels demonstrate various sub-conductance levels. When a channel is open, ions permeate through the channel pore down the transmembrane concentration gradient for that particular ion. Rate of ionic flow through the channel, i.e. single-channel current amplitude, is determined by the maximum channel conductance and electrochemical driving force for that ion, which is the difference between the instantaneous value of the membrane potential and the value of the reversal potential.^[18]

Depiction of the open potassium channel, with the potassium ion shown in purple in the middle, and hydrogen atoms omitted. When the channel is closed, the passage is blocked.

A channel may have several different states (corresponding to different conformations of the protein), but each such state is either open or closed. In general, closed states correspond either to a contraction of the pore—making it impassable to the ion—or to a separate part of the protein, stoppering the pore. For example, the voltage-dependent sodium channel undergoes inactivation, in which a portion of the protein swings into the pore, sealing it.^[19] This inactivation shuts off the sodium current and plays a critical role in the action potential.

Ion channels can be classified by how they respond to their environment.^[20] For example, the ion channels involved in the action potential are voltage-sensitive channels; they open and close in response to the voltage across the membrane. Ligand-gated channels form another important class; these ion channels open and close in response to the binding of a ligand molecule, such as a neurotransmitter. Other ion channels open and close with mechanical forces. Still other ion channels—such as those of sensory neurons—open and close in response to other stimuli, such as light, temperature or pressure.

Leakage channels

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Leakage channels are the simplest type of ion channel, in that their permeability is more or less constant. The types of leakage channels that have the greatest significance in neurons are potassium and chloride channels. Even these are not perfectly constant in their properties: First, most of them are voltage-dependent in the sense that they conduct better in one direction than the other (in other words, they are rectifiers); second, some of them are capable of being shut off by chemical ligands even though they do not require ligands in order to operate.

Ligand-gated channels

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Ligand-gated calcium channel in closed and open states

Ligand-gated ion channels are channels whose permeability is greatly increased when some type of chemical ligand binds to the protein structure. Animal cells contain hundreds, if not thousands, of types of these. A large subset function as neurotransmitter receptors—they occur at postsynaptic sites, and the chemical ligand that gates them is released by the presynaptic axon terminal. One example of this type is the AMPA receptor, a receptor for the neurotransmitter glutamate that when activated allows passage of sodium and potassium ions. Another example is the GABA_A receptor, a receptor for the neurotransmitter GABA that when activated allows passage of chloride ions.

Neurotransmitter receptors are activated by ligands that appear in the extracellular area, but there are other types of ligand-gated channels that are controlled by interactions on the intracellular side.

Voltage-dependent channels

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Voltage-gated ion channels, also known as voltage dependent ion channels, are channels whose permeability is influenced by the membrane potential. They form another very large group, with each member having a particular ion selectivity and a particular voltage dependence. Many are also time-dependent—in other words, they do not respond immediately to a voltage change but only after a delay.

One of the most important members of this group is a type of voltage-gated sodium channel that underlies action potentials—these are sometimes called Hodgkin-Huxley sodium channels because they were initially characterized by Alan Lloyd Hodgkin and Andrew Huxley in their Nobel Prize-winning studies of the physiology of the action potential. The channel is closed at the resting voltage level, but opens abruptly when the voltage exceeds a certain threshold, allowing a large influx of sodium ions that produces a very rapid change in the membrane potential. Recovery from an action potential is partly dependent on a type of voltage-gated potassium channel that is closed at the resting voltage level but opens as a consequence of the large voltage change produced during the action potential.

Reversal potential

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The reversal potential (or equilibrium potential) of an ion is the value of transmembrane voltage at which diffusive and electrical forces counterbalance, so that there is no net ion flow across the membrane. This means that the transmembrane voltage exactly opposes the force of diffusion of the ion, such that the net current of the ion across the membrane is zero and unchanging. The reversal potential is important because it gives the voltage that acts on channels permeable to that ion—in other words, it gives the voltage that the ion concentration gradient generates when it acts as a battery.

The equilibrium potential of a particular ion is usually designated by the notation E_ion.The equilibrium potential for any ion can be calculated using the Nernst equation.^[21] For example, reversal potential for potassium ions will be as follows:

${\displaystyle E_{eq,K^{+}}=\frac{RT}{zF}\ln \frac{[K^{+}{]}_o}{[K^{+}{]}_i}}$

where

• E_eq,K⁺= equilibrium potential for potassium, measured in volts
• R = universal gas constant, equal to 8.314 joules·K⁻¹·mol⁻¹
• T = absolute temperature, measured in kelvins (= K = degrees Celsius + 273.15)
• z = number of elementary charges of the ion in question involved in the reaction
• F = Faraday constant, equal to 96,485 coulombs·mol⁻¹ or J·V⁻¹·mol⁻¹
• [K⁺]_o= extracellular concentration of potassium, measured in mol·m⁻³ or mmol·l⁻¹
• [K⁺]_i= intracellular concentration of potassium

Even if two different ions have the same charge (i.e., K⁺ and Na⁺), they can still have very different equilibrium potentials, provided their outside and/or inside concentrations differ. Take, for example, the equilibrium potentials of potassium and sodium in neurons. The potassium equilibrium potential E_K is −84 mV with 5 mM potassium outside and 140 mM inside. On the other hand, the sodium equilibrium potential, E_Na, is approximately +66 mV with approximately 12 mM sodium inside and 140 mM outside.^{[note 1]}

Changes to membrane potential during development

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A neuron's resting membrane potential actually changes during the development of an organism. In order for a neuron to eventually adopt its full adult function, its potential must be tightly regulated during development. As an organism progresses through development the resting membrane potential becomes more negative.^[22] Glial cells are also differentiating and proliferating as development progresses in the brain.^[23] The addition of these glial cells increases the organism's ability to regulate extracellular potassium. The drop in extracellular potassium can lead to a decrease in membrane potential of 35 mV.^[24]

Cell excitability

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Further information: Excitable medium

Cell excitability is the change in membrane potential that is necessary for cellular responses in various tissues. Cell excitability is a property that is induced during early embriogenesis.^[25] Excitability of a cell has also been defined as the ease with which a response may be triggered.^[26] The resting and threshold potentials forms the basis of cell excitability and these processes are fundamental for the generation of graded and action potentials.

The most important regulators of cell excitability are the extracellular electrolyte concentrations (i.e. Na⁺, K⁺, Ca²⁺, Cl⁻, Mg²⁺) and associated proteins. Important proteins that regulate cell excitability are voltage-gated ion channels, ion transporters (e.g. Na+/K+-ATPase, magnesium transporters, acid–base transporters), membrane receptors and hyperpolarization-activated cyclic-nucleotide-gated channels.^[27] For example, potassium channels and calcium-sensing receptors are important regulators of excitability in neurons, cardiac myocytes and many other excitable cells like astrocytes.^[28] Calcium ion is also the most important second messenger in excitable cell signaling. Activation of synaptic receptors initiates long-lasting changes in neuronal excitability.^[29] Thyroid, adrenal and other hormones also regulate cell excitability, for example, progesterone and estrogen modulate myometrial smooth muscle cell excitability.

Many cell types are considered to have an excitable membrane. Excitable cells are neurons, muscle (cardiac, skeletal, smooth), vascular endothelial cells, pericytes, juxtaglomerular cells, interstitial cells of Cajal, many types of epithelial cells (e.g. beta cells, alpha cells, delta cells, enteroendocrine cells, pulmonary neuroendocrine cells, pinealocytes), glial cells (e.g. astrocytes), mechanoreceptor cells (e.g. hair cells and Merkel cells), chemoreceptor cells (e.g. glomus cells, taste receptors), some plant cells and possibly immune cells.^[30] Astrocytes display a form of non-electrical excitability based on intracellular calcium variations related to the expression of several receptors through which they can detect the synaptic signal. In neurons, there are different membrane properties in some portions of the cell, for example, dendritic excitability endows neurons with the capacity for coincidence detection of spatially separated inputs.^[31]

	Name of the deity	Identified with	Sin		Name of the deity	Identified with	Sin
1	Usekh-nemmt "Far-Strider"	Heliopolis	falsehood	22	Maa-antuf "Demolisher"	Xois	Transgressing
2	Hept-khet "Fire-Embracer"	Kheraha (Old Cairo?[13])	Robbery	23	Her-uru "Disturber"	Weryt	Being hot-tempered
3	Fenti "Nosey One"	Hermopolis	Stealing	24	Khemiu "Youth"	Heliopolitan nome	Unhearing of truth
4	Am-khaibit "Swallower of Shades"	"The Cavern"	Murder	25	Shet-kheru "Foreteller"	Wenes	Making disturbance
5	Neha-her "Dangerous One"	Rosetau (Giza Plateau[14])	Stealing grain	26	Nebheru "You of the Altar"	"the secret place"	Violence
6	Ruruti "Double Lion"	"The sky"	Purloined offerings	27[15]	Kenemti "Face Behind Him"	"Cavern of wrong"	copulating with a boy
7	Arfi-em-khet "Fiery Eyes"	Letopolis	Stealing Gods property	28	An-hetep-f "Hot-Foot"	"The dusk"	Transgression
8	Neba "Flame"	"Came forth backwards"	Lying	29	Sera-kheru "You of the Darkness"	"The darkness"	Quarrelling
9	Set-qesu "Bone Breaker"	Heracleopolis	Taking food	30	Neb-heru "Bringer of Your Offerings"	Sais	Unduly active
10	Utu-nesert "Green of Flame"	Memphis	Cursing	31	Sekhriu "Owner of Faces"	Nedjefet (13th / 14th Upper Egyptian nome)	Impatience
11	Qerrti "You of the Cavern"	"The West"	Adultery	32	Neb-abui "Accuser"	Wetjenet (in Punt[16])	damaging a god's image
12	Hraf-haf "White of Teeth"	Faiyum	Causing tears	33	"Owner of Horns"	Asyut	Volubility of speech
13	Hetch-abhu/ Shezmu "House of Nature"	"The shambles"	Killing a sacred bull	34	Nefertem	Memphis	Wrongdoing
14	Ta-retiu "Eater of Entrails"	"House of Thirty"	Stealing land	35	Temsep/Tem-Sepu	Busiris	Conjuration against the king
15	Unem-snef "Lord of Truth"	Maaty	Eavesdropping	36	Ari-em-ab-f "You Who Acted Willfully"	Tjebu	Stopping water flow
16	Unem-besek "Wanderer"	Bubastis	Complaints	37	Ahi "Water-Smiter"	"The abyss"	Being loud voiced
17	Neb-Maat "Pale One"	Heliopolis	Being angry	38	Uatch-rekhit "Commander of Mankind"	"Your house"	Reviling God
18	Tenemiu "Doubly Evil"	Andjet	Adultery	39	Nehebkau	The Harpoon Nome (7th / 8th Lower Egyptian nome[17])	Arrogance
19	Sertiu "Wememty-Snake"	"Place of execution"	Adultery	40	Neheb-nefert Bestower of Powers"	"The city"	Making distinctions For self
20	Tutu "See Whom You Bring"	"House of Min"	Polluting the body	41	Hetch-abhu "Serpent With Raised Head"	"The cavern"	dishonest wealth
21	Uamenti "Over the Old One"	Imau	Terrorizing	42	Neb-abui "Serpent Who Brings and Gives"	"The silent land"	Blasphemy

Equivalent circuit

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Equivalent circuit for a patch of membrane, consisting of a fixed capacitance in parallel with four pathways each containing a battery in series with a variable conductance

Electrophysiologists model the effects of ionic concentration differences, ion channels, and membrane capacitance in terms of an equivalent circuit, which is intended to represent the electrical properties of a small patch of membrane. The equivalent circuit consists of a capacitor in parallel with four pathways each consisting of a battery in series with a variable conductance. The capacitance is determined by the properties of the lipid bilayer, and is taken to be fixed. Each of the four parallel pathways comes from one of the principal ions, sodium, potassium, chloride, and calcium. The voltage of each ionic pathway is determined by the concentrations of the ion on each side of the membrane; see the Reversal potential section above. The conductance of each ionic pathway at any point in time is determined by the states of all the ion channels that are potentially permeable to that ion, including leakage channels, ligand-gated channels, and voltage-gated ion channels.

Reduced circuit obtained by combining the ion-specific pathways using the Goldman equation

For fixed ion concentrations and fixed values of ion channel conductance, the equivalent circuit can be further reduced, using the Goldman equation as described below, to a circuit containing a capacitance in parallel with a battery and conductance. In electrical terms, this is a type of RC circuit (resistance-capacitance circuit), and its electrical properties are very simple. Starting from any initial state, the current flowing across either the conductance or the capacitance decays with an exponential time course, with a time constant of τ = RC, where C is the capacitance of the membrane patch, and R = 1/g_net is the net resistance. For realistic situations, the time constant usually lies in the 1—100 millisecond range. In most cases, changes in the conductance of ion channels occur on a faster time scale, so an RC circuit is not a good approximation; however, the differential equation used to model a membrane patch is commonly a modified version of the RC circuit equation.

Resting potential

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When the membrane potential of a cell goes for a long period of time without changing significantly, it is referred to as a resting potential or resting voltage. This term is used for the membrane potential of non-excitable cells, but also for the membrane potential of excitable cells in the absence of excitation. In excitable cells, the other possible states are graded membrane potentials (of variable amplitude), and action potentials, which are large, all-or-nothing rises in membrane potential that usually follow a fixed time course. Excitable cells include neurons, muscle cells, and some secretory cells in glands. Even in other types of cells, however, the membrane voltage can undergo changes in response to environmental or intracellular stimuli. For example, depolarization of the plasma membrane appears to be an important step in programmed cell death.^[32]

The interactions that generate the resting potential are modeled by the Goldman equation.^[33] This is similar in form to the Nernst equation shown above, in that it is based on the charges of the ions in question, as well as the difference between their inside and outside concentrations. However, it also takes into consideration the relative permeability of the plasma membrane to each ion in question.

${\displaystyle E_m=\frac{RT}{F}\ln \left(\frac{P_{\mathrm{K}}[{\mathrm{K}}^{+}{]}_{\mathrm{o}\mathrm{u}\mathrm{t}}+P_{\mathrm{N}\mathrm{a}}[{\mathrm{N}\mathrm{a}}^{+}{]}_{\mathrm{o}\mathrm{u}\mathrm{t}}+P_{\mathrm{C}\mathrm{l}}[{\mathrm{C}\mathrm{l}}^{-}{]}_{\mathrm{i}\mathrm{n}}}{P_{\mathrm{K}}[{\mathrm{K}}^{+}{]}_{\mathrm{i}\mathrm{n}}+P_{\mathrm{N}\mathrm{a}}[{\mathrm{N}\mathrm{a}}^{+}{]}_{\mathrm{i}\mathrm{n}}+P_{\mathrm{C}\mathrm{l}}[{\mathrm{C}\mathrm{l}}^{-}{]}_{\mathrm{o}\mathrm{u}\mathrm{t}}}\right)}$

The three ions that appear in this equation are potassium (K⁺), sodium (Na⁺), and chloride (Cl⁻). Calcium is omitted, but can be added to deal with situations in which it plays a significant role.^[34] Being an anion, the chloride terms are treated differently from the cation terms; the intracellular concentration is in the numerator, and the extracellular concentration in the denominator, which is reversed from the cation terms. P_i stands for the relative permeability of the ion type i.

In essence, the Goldman formula expresses the membrane potential as a weighted average of the reversal potentials for the individual ion types, weighted by permeability. (Although the membrane potential changes about 100 mV during an action potential, the concentrations of ions inside and outside the cell do not change significantly. They remain close to their respective concentrations when then membrane is at resting potential.) In most animal cells, the permeability to potassium is much higher in the resting state than the permeability to sodium. As a consequence, the resting potential is usually close to the potassium reversal potential.^[35][36] The permeability to chloride can be high enough to be significant, but, unlike the other ions, chloride is not actively pumped, and therefore equilibrates at a reversal potential very close to the resting potential determined by the other ions.

Values of resting membrane potential in most animal cells usually vary between the potassium reversal potential (usually around -80 mV) and around -40 mV. The resting potential in excitable cells (capable of producing action potentials) is usually near -60 mV—more depolarized voltages would lead to spontaneous generation of action potentials. Immature or undifferentiated cells show highly variable values of resting voltage, usually significantly more positive than in differentiated cells.^[37] In such cells, the resting potential value correlates with the degree of differentiation: undifferentiated cells in some cases may not show any transmembrane voltage difference at all.

Maintenance of the resting potential can be metabolically costly for a cell because of its requirement for active pumping of ions to counteract losses due to leakage channels. The cost is highest when the cell function requires an especially depolarized value of membrane voltage. For example, the resting potential in daylight-adapted blowfly (Calliphora vicina) photoreceptors can be as high as -30 mV.^[38] This elevated membrane potential allows the cells to respond very rapidly to visual inputs; the cost is that maintenance of the resting potential may consume more than 20% of overall cellular ATP.^[39]

On the other hand, the high resting potential in undifferentiated cells does not necessarily incur a high metabolic cost. This apparent paradox is resolved by examination of the origin of that resting potential. Little-differentiated cells are characterized by extremely high input resistance,^[37] which implies that few leakage channels are present at this stage of cell life. As an apparent result, potassium permeability becomes similar to that for sodium ions, which places resting potential in-between the reversal potentials for sodium and potassium as discussed above. The reduced leakage currents also mean there is little need for active pumping in order to compensate, therefore low metabolic cost.

Graded potentials

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As explained above, the potential at any point in a cell's membrane is determined by the ion concentration differences between the intracellular and extracellular areas, and by the permeability of the membrane to each type of ion. The ion concentrations do not normally change very quickly (with the exception of Ca²⁺, where the baseline intracellular concentration is so low that even a small influx may increase it by orders of magnitude), but the permeabilities of the ions can change in a fraction of a millisecond, as a result of activation of ligand-gated ion channels. The change in membrane potential can be either large or small, depending on how many ion channels are activated and what type they are, and can be either long or short, depending on the lengths of time that the channels remain open. Changes of this type are referred to as graded potentials, in contrast to action potentials, which have a fixed amplitude and time course.

As can be derived from the Goldman equation shown above, the effect of increasing the permeability of a membrane to a particular type of ion shifts the membrane potential toward the reversal potential for that ion. Thus, opening Na⁺ channels shifts the membrane potential toward the Na⁺ reversal potential, which is usually around +100 mV. Likewise, opening K⁺ channels shifts the membrane potential toward about –90 mV, and opening Cl⁻ channels shifts it toward about –70 mV (resting potential of most membranes). Thus, Na⁺ channels shift the membrane potential in a positive direction, K⁺ channels shift it in a negative direction (except when the membrane is hyperpolarized to a value more negative than the K⁺ reversal potential), and Cl⁻ channels tend to shift it towards the resting potential.

Graph displaying an EPSP, an IPSP, and the summation of an EPSP and an IPSP

Graded membrane potentials are particularly important in neurons, where they are produced by synapses—a temporary change in membrane potential produced by activation of a synapse by a single graded or action potential is called a postsynaptic potential. Neurotransmitters that act to open Na⁺ channels typically cause the membrane potential to become more positive, while neurotransmitters that activate K⁺ channels typically cause it to become more negative; those that inhibit these channels tend to have the opposite effect.

Whether a postsynaptic potential is considered excitatory or inhibitory depends on the reversal potential for the ions of that current, and the threshold for the cell to fire an action potential (around –50mV). A postsynaptic current with a reversal potential above threshold, such as a typical Na⁺ current, is considered excitatory. A current with a reversal potential below threshold, such as a typical K⁺ current, is considered inhibitory. A current with a reversal potential above the resting potential, but below threshold, will not by itself elicit action potentials, but will produce subthreshold membrane potential oscillations. Thus, neurotransmitters that act to open Na⁺ channels produce excitatory postsynaptic potentials, or EPSPs, whereas neurotransmitters that act to open K⁺ or Cl⁻ channels typically produce inhibitory postsynaptic potentials, or IPSPs. When multiple types of channels are open within the same time period, their postsynaptic potentials summate (are added together).

Other values

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From the viewpoint of biophysics, the resting membrane potential is merely the membrane potential that results from the membrane permeabilities that predominate when the cell is resting. The above equation of weighted averages always applies, but the following approach may be more easily visualized. At any given moment, there are two factors for an ion that determine how much influence that ion will have over the membrane potential of a cell:

1. That ion's driving force
2. That ion's permeability

If the driving force is high, then the ion is being "pushed" across the membrane. If the permeability is high, it will be easier for the ion to diffuse across the membrane.

• Driving force is the net electrical force available to move that ion across the membrane. It is calculated as the difference between the voltage that the ion "wants" to be at (its equilibrium potential) and the actual membrane potential (E_m). So, in formal terms, the driving force for an ion = E_m - E_ion
• For example, at our earlier calculated resting potential of −73 mV, the driving force on potassium is 7 mV : (−73 mV) − (−80 mV) = 7 mV. The driving force on sodium would be (−73 mV) − (60 mV) = −133 mV.
• Permeability is a measure of how easily an ion can cross the membrane. It is normally measured as the (electrical) conductance and the unit, siemens, corresponds to 1 C·s⁻¹·V⁻¹, that is one coulomb per second per volt of potential.

So, in a resting membrane, while the driving force for potassium is low, its permeability is very high. Sodium has a huge driving force but almost no resting permeability. In this case, potassium carries about 20 times more current than sodium, and thus has 20 times more influence over E_m than does sodium.

However, consider another case—the peak of the action potential. Here, permeability to Na is high and K permeability is relatively low. Thus, the membrane moves to near E_Na and far from E_K.

The more ions are permeant the more complicated it becomes to predict the membrane potential. However, this can be done using the Goldman-Hodgkin-Katz equation or the weighted means equation. By plugging in the concentration gradients and the permeabilities of the ions at any instant in time, one can determine the membrane potential at that moment. What the GHK equations means is that, at any time, the value of the membrane potential will be a weighted average of the equilibrium potentials of all permeant ions. The "weighting" is the ions relative permeability across the membrane.

Effects and implications

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While cells expend energy to transport ions and establish a transmembrane potential, they use this potential in turn to transport other ions and metabolites such as sugar. The transmembrane potential of the mitochondria drives the production of ATP, which is the common currency of biological energy.

Cells may draw on the energy they store in the resting potential to drive action potentials or other forms of excitation. These changes in the membrane potential enable communication with other cells (as with action potentials) or initiate changes inside the cell, which happens in an egg when it is fertilized by a sperm.

Changes in the dielectric properties of plasma membrane may act as hallmark of underlying conditions such as diabetes and dyslipidemia.^[40]

In neuronal cells, an action potential begins with a rush of sodium ions into the cell through sodium channels, resulting in depolarization, while recovery involves an outward rush of potassium through potassium channels. Both of these fluxes occur by passive diffusion.

A dose of salt may trigger the still-working neurons of a fresh cut of meat into firing, causing muscle spasms.^{[41][42][43][44][45]}

See also

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• Bioelectrochemistry
• Chemiosmotic potential
• Electrochemical potential
• Goldman equation
• Membrane biophysics
• Microelectrode array
• Saltatory conduction
• Surface potential
• Gibbs–Donnan effect
• Synaptic potential

Notes

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1. ^ The signs of E_Na and E_K are opposite. This is because the concentration gradient for potassium is directed out of the cell, while the concentration gradient for sodium is directed into the cell. Membrane potentials are defined relative to the exterior of the cell; thus, a potential of −70 mV implies that the interior of the cell is negative relative to the exterior.

References

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4. ^ Campbell Biology, 6th edition
5. ^ Johnston and Wu, p. 9.
6. ^ Jump up to:^a b Bullock, Orkand, and Grinnell, pp. 140–41.
7. ^ Bullock, Orkand, and Grinnell, pp. 153–54.
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14. ^ Steinbach HB, Spiegelman S (1943). "The sodium and potassium balance in squid nerve axoplasm". J. Cell. Comp. Physiol. 22 (2): 187–96. doi:10.1002/jcp.1030220209.
15. ^ Jump up to:^a b Hodgkin AL (1951). "The ionic basis of electrical activity in nerve and muscle". Biol. Rev. 26 (4): 339–409. doi:10.1111/j.1469-185X.1951.tb01204.x. S2CID 86282580.
16. ^ CRC Handbook of Chemistry and Physics, 83rd edition, ISBN 0-8493-0483-0, pp. 12–14 to 12–16.
17. ^ Eisenman G (1961). "On the elementary atomic origin of equilibrium ionic specificity". In A Kleinzeller; A Kotyk (eds.). Symposium on Membrane Transport and Metabolism. New York: Academic Press. pp. 163–79.Eisenman G (1965). "Some elementary factors involved in specific ion permeation". Proc. 23rd Int. Congr. Physiol. Sci., Tokyo. Amsterdam: Excerta Med. Found. pp. 489–506.
    * Diamond JM, Wright EM (1969). "Biological membranes: the physical basis of ion and nonekectrolyte selectivity". Annual Review of Physiology. 31: 581–646. doi:10.1146/annurev.ph.31.030169.003053. PMID 4885777.
18. ^ Junge, pp. 33–37.
19. ^ Cai SQ, Li W, Sesti F (2007). "Multiple modes of a-type potassium current regulation". Curr. Pharm. Des. 13 (31): 3178–84. doi:10.2174/138161207782341286. PMID 18045167.
20. ^ Goldin AL (2007). "Neuronal Channels and Receptors". In Waxman SG (ed.). Molecular Neurology. Burlington, MA: Elsevier Academic Press. pp. 43–58. ISBN 978-0-12-369509-3.
21. ^ Purves et al., pp. 28–32; Bullock, Orkand, and Grinnell, pp. 133–134; Schmidt-Nielsen, pp. 478–480, 596–597; Junge, pp. 33–35
22. ^ Sanes, Dan H.; Takács, Catherine (1993-06-01). "Activity-dependent Refinement of Inhibitory Connections". European Journal of Neuroscience. 5 (6): 570–574. doi:10.1111/j.1460-9568.1993.tb00522.x. ISSN 1460-9568. PMID 8261131. S2CID 30714579.
23. ^ KOFUJI, P.; NEWMAN, E. A. (2004-01-01). "Potassium buffering in the central nervous system". Neuroscience. 129 (4): 1045–1056. doi:10.1016/j.neuroscience.2004.06.008. ISSN 0306-4522. PMC 2322935. PMID 15561419.
24. ^ Sanes, Dan H.; Reh, Thomas A (2012-01-01). Development of the nervous system (Third ed.). Elsevier Academic Press. pp. 211–214. ISBN 9780080923208. OCLC 762720374.
25. ^ Tosti, Elisabetta (2010-06-28). "Dynamic roles of ion currents in early development". Molecular Reproduction and Development. 77 (10): 856–867. doi:10.1002/mrd.21215. ISSN 1040-452X. PMID 20586098. S2CID 38314187.
26. ^ Boyet, M.R.; Jewell, B.R. (1981). "Analysis of the effects of changes in rate and rhythm upon electrical activity in the heart". Progress in Biophysics and Molecular Biology. 36 (1): 1–52. doi:10.1016/0079-6107(81)90003-1. ISSN 0079-6107. PMID 7001542.
27. ^ Spinelli, Valentina; Sartiani, Laura; Mugelli, Alessandro; Romanelli, Maria Novella; Cerbai, Elisabetta (2018). "Hyperpolarization-activated cyclic-nucleotide-gated channels: pathophysiological, developmental, and pharmacological insights into their function in cellular excitability". Canadian Journal of Physiology and Pharmacology. 96 (10): 977–984. doi:10.1139/cjpp-2018-0115. hdl:1807/90084. ISSN 0008-4212. PMID 29969572. S2CID 49679747.
28. ^ Jones, Brian L.; Smith, Stephen M. (2016-03-30). "Calcium-Sensing Receptor: A Key Target for Extracellular Calcium Signaling in Neurons". Frontiers in Physiology. 7: 116. doi:10.3389/fphys.2016.00116. ISSN 1664-042X. PMC 4811949. PMID 27065884.
29. ^ Debanne, Dominique; Inglebert, Yanis; Russier, Michaël (2019). "Plasticity of intrinsic neuronal excitability" (PDF). Current Opinion in Neurobiology. 54: 73–82. doi:10.1016/j.conb.2018.09.001. PMID 30243042. S2CID 52812190.
30. ^ Davenport, Bennett; Li, Yuan; Heizer, Justin W.; Schmitz, Carsten; Perraud, Anne-Laure (2015-07-23). "Signature Channels of Excitability no More: L-Type Channels in Immune Cells". Frontiers in Immunology. 6: 375. doi:10.3389/fimmu.2015.00375. ISSN 1664-3224. PMC 4512153. PMID 26257741.
31. ^ Sakmann, Bert (2017-04-21). "From single cells and single columns to cortical networks: dendritic excitability, coincidence detection and synaptic transmission in brain slices and brains". Experimental Physiology. 102 (5): 489–521. doi:10.1113/ep085776. ISSN 0958-0670. PMC 5435930. PMID 28139019.
32. ^ Franco R, Bortner CD, Cidlowski JA (January 2006). "Potential roles of electrogenic ion transport and plasma membrane depolarization in apoptosis". J. Membr. Biol. 209 (1): 43–58. doi:10.1007/s00232-005-0837-5. PMID 16685600. S2CID 849895.
33. ^ Purves et al., pp. 32–33; Bullock, Orkand, and Grinnell, pp. 138–140; Schmidt-Nielsen, pp. 480; Junge, pp. 35–37
34. ^ Spangler SG (1972). "Expansion of the constant field equation to include both divalent and monovalent ions". Alabama Journal of Medical Sciences. 9 (2): 218–23. PMID 5045041.
35. ^ Purves et al., p. 34; Bullock, Orkand, and Grinnell, p. 134; Schmidt-Nielsen, pp. 478–480.
36. ^ Purves et al., pp. 33–36; Bullock, Orkand, and Grinnell, p. 131.
37. ^ Jump up to:^a b Magnuson DS, Morassutti DJ, Staines WA, McBurney MW, Marshall KC (Jan 14, 1995). "In vivo electrophysiological maturation of neurons derived from a multipotent precursor (embryonal carcinoma) cell line". Developmental Brain Research. 84 (1): 130–41. doi:10.1016/0165-3806(94)00166-W. PMID 7720212.
38. ^ Juusola M, Kouvalainen E, Järvilehto M, Weckström M (Sep 1994). "Contrast gain, signal-to-noise ratio, and linearity in light-adapted blowfly photoreceptors". J Gen Physiol. 104 (3): 593–621. doi:10.1085/jgp.104.3.593. PMC 2229225. PMID 7807062.
39. ^ Laughlin SB, de Ruyter van Steveninck RR, Anderson JC (May 1998). "The metabolic cost of neural information". Nat. Neurosci. 1 (1): 36–41. doi:10.1038/236. PMID 10195106. S2CID 204995437.
40. ^ Ghoshal K, et al. (December 2017). "Dielectric properties of plasma membrane: A signature for dyslipidemia in diabetes mellitus". Arch Biochem Biophys. 635: 27–36. doi:10.1016/j.abb.2017.10.002. PMID 29029878.
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Further reading

[edit]

• Alberts et al. Molecular Biology of the Cell. Garland Publishing; 4th Bk&Cdr edition (March, 2002). ISBN 0-8153-3218-1. Undergraduate level.
• Guyton, Arthur C., John E. Hall. Textbook of medical physiology. W.B. Saunders Company; 10th edition (August 15, 2000). ISBN 0-7216-8677-X. Undergraduate level.
• Hille, B. Ionic Channel of Excitable Membranes Sinauer Associates, Sunderland, MA, USA; 1st Edition, 1984. ISBN 0-87893-322-0
• Nicholls, J.G., Martin, A.R. and Wallace, B.G. From Neuron to Brain Sinauer Associates, Inc. Sunderland, MA, USA 3rd Edition, 1992. ISBN 0-87893-580-0
• Ove-Sten Knudsen. Biological Membranes: Theory of Transport, Potentials and Electric Impulses. Cambridge University Press (September 26, 2002). ISBN 0-521-81018-3. Graduate level.
• National Medical Series for Independent Study. Physiology. Lippincott Williams & Wilkins. Philadelphia, PA, USA 4th Edition, 2001. ISBN 0-683-30603-0

External links

[edit]

• Functions of the Cell Membrane
• Nernst/Goldman Equation Simulator
• Nernst Equation Calculator
• Goldman-Hodgkin-Katz Equation Calculator
• Electrochemical Driving Force Calculator
• The Origin of the Resting Membrane Potential - Online interactive tutorial (Flash)

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Categories: 

• Cell communication
• Cell signaling
• Cellular processes
• Cellular neuroscience
• Electrochemical concepts
• Electrophysiology
• Membrane biology

• This page was last edited on 20 August 2024, at 01:06 (UTC).

• Each of the four homologous domains makes up one subunit of the ion channel. The S4 voltage-sensing segments (marked with + symbols) are shown as charged.
  Identifiers
  Symbol	VIC
  Pfam clan	CL0030
  TCDB	1.A.1
  OPM superfamily	8
  OPM protein	2a79

  

  Ions are depicted by the red circles. A gradient is represented by the different concentration of ions on either side of the membrane. The open conformation of the ion channel allows for the translocation of ions across the cell membrane, while the closed conformation does not.

• Voltage-gated ion channels are a class of transmembrane proteins that form ion channels that are activated by changes in a cell's electrical membrane potential near the channel. The membrane potential alters the conformation of the channel proteins, regulating their opening and closing. Cell membranes are generally impermeable to ions, thus they must diffuse through the membrane through transmembrane protein channels.

  Voltage-gated ion channels have a crucial role in excitable cells such as neuronal and muscle tissues, allowing a rapid and co-ordinated depolarization in response to triggering voltage change. Found along the axon and at the synapse, voltage-gated ion channels directionally propagate electrical signals.

  Voltage-gated ion-channels are usually ion-specific, and channels specific to sodium (Na⁺), potassium (K⁺), calcium (Ca²⁺), and chloride (Cl⁻) ions have been identified.^[1] The opening and closing of the channels are triggered by changing ion concentration, and hence charge gradient, between the sides of the cell membrane.^[2]

• Voltage-gated ion channels are generally composed of several subunits arranged in such a way that there is a central pore through which ions can travel down their electrochemical gradients. The channels tend to be ion-specific, although similarly sized and charged ions may sometimes travel through them.

  The functionality of voltage-gated ion channels is attributed to its three main discrete units: the voltage sensor, the pore or conducting pathway, and the gate.^[3] Na⁺, K⁺, and Ca²⁺ channels are composed of four transmembrane domains arranged around a central pore; these four domains are part of a single α-subunit in the case of most Na⁺ and Ca²⁺ channels, whereas there are four α-subunits, each contributing one transmembrane domain, in most K⁺ channels.^[4]

  The membrane-spanning segments, designated S1-S6, all take the form of alpha helices with specialized functions. The fifth and sixth transmembrane segments (S5 and S6) and pore loop serve the principal role of ion conduction, comprising the gate and pore of the channel, while S1-S4 serve as the voltage-sensing region.^[3]

  The four subunits may be identical, or different from one another. In addition to the four central α-subunits, there are also regulatory β-subunits, with oxidoreductase activity, which are located on the inner surface of the cell membrane and do not cross the membrane, and which are coassembled with the α-subunits in the endoplasmic reticulum.^[5]

• From Wikipedia, the free encyclopedia

  A microcurrent electrical neuromuscular stimulator or MENS (also microamperage electrical neuromuscular stimulator) is a device used to send weak electrical signals into the body. Such devices apply extremely small microamp [uA] electrical currents (less than 1 milliampere [mA]) to the tissues using electrodes placed on the skin. One microampere [uA] is 1 millionth of an ampere and the uses of MENS are distinct from those of "TENS" which runs at one milliamp [mA] or one thousandth of an amp.

  Uses

  [edit]

  MENS uses include treatments for pain,^[1] diabetic neuropathy,^[2] age-related macular degeneration, wound healing, tendon repair, plantar fasciitis^[3] and ruptured ligament recovery. Most microcurrent treatments concentrate on pain and/or speeding healing and recovery.^[4] It is commonly used by professional and performance athletes with acute pain and/or muscle tenderness as it is drug-free and non-invasive, thus avoiding testing and recovery issues. It is also used as a cosmetic treatment.^[5]

  History

  [edit]

  The body's electrical capabilities were studied at least as early as 1830, when the Italian Carlo Matteucci is credited as being one of the first to measure the electrical current in injured tissue. Bioelectricity received less attention after the discovery of penicillin, when the focus of medical research and treatments turned toward the body's chemical processes.^[6] Attention began to return to these properties and the possibilities of using very low current for healing in the mid-1900s. In a study published in 1969, for example, a team of researchers led by L.E. Wolcott applied microcurrent to a wide variety of wounds, using negative polarity over lesions in the initial phase, and then alternating application of positive and negative electrodes every three days. The stimulation current ranged from 200 to 800 uA and the treated group showed 200%-350% faster healing rates, with stronger tensile strength of scar tissue and antibacterial effects.^[7]

  In 1991, the German scientists Drs. Erwin Neher and Bert Sakmann shared the Nobel Prize in Physiology or Medicine for their development of the patch-clamp technique that allows the detection of minute electrical currents through cell membranes. This method allowed the detection of more than 20 different types of ion channel which permit positive or negatively charged ions to cross the cell membrane, confirming that cellular electrical activity is not limited only to nerve and muscle tissues.^{[citation needed]}

• The ethmoid sinuses or ethmoid air cells of the ethmoid bone are one of the four paired paranasal sinuses.^[1] Unlike the other three pairs of paranasal sinuses which consist of one or two large cavities, the ethmoidal sinuses entail a number of small air-filled cavities ("air cells").^[2] The cells are located within the lateral mass (labyrinth) of each ethmoid bone and are variable in both size and number.^[1] The cells are grouped into anterior, middle, and posterior groups; the groups differ in their drainage modalities,^[2] though all ultimately drain into either the superior or the middle nasal meatus^[3] of the lateral wall of the nasal cavity.

  Structure

  [edit]

  The ethmoid air cells consist of numerous thin-walled cavities in the ethmoidal labyrinth^[4] that represent invaginations of the mucous membrane of the nasal wall into the ethmoid bone.^[3] They are situated between the superior parts of the nasal cavities and the orbits, and are separated from these cavities by thin bony lamellae.^[4]

  There are 5-15 air cells in either ethmoid bone in the adult, with a combined volume of 2-3mL.^[5]

  Development

  [edit]

  The ethmoidal cells (sinuses) and maxillary sinuses are present at birth.^[6] At birth, 3-4 air cells are present, with the number increasing to 5-15 by adulthood.^[5]

  Drainage

  [edit]
  • The anterior ethmoidal cells drain (directly or indirectly^[3]) into the middle nasal meatus by way of the ethmoidal infundibulum.^[4][3][5]
  • The middle ethmoidal cells drain directly into the middle nasal meatus.^[3]
  • The posterior ethmoidal cells drain directly into the superior nasal meatus^[3][5] at the sphenoethmoidal recess;^[5] sometimes, one or more opens into the sphenoidal sinus.^[4]

  Lamellae

  [edit]

  The ethmoidal labyrinth is divided by multiple obliquely oriented, parallel lamellae. The first lamellae is equivalent to the uncinate process of ethmoid bone, the second corresponds the ethmoid bulla, and the third is the basal lamella, and the fourth is equivalent to the superior nasal concha.^[5]

  The anterior and posterior ethmoid cells are separated by the basal lamella^[7][5] (also known as the ground lamella).^[5] It is one of the bony divisions of the ethmoid bone and is mostly contained inside the ethmoid labyrinth. The basal lamella is continuous medially with the bony middle nasal concha.^[7] Anteriorly, it vertically inserts into the ethmoid crest; the middle part attaches obliquely into the orbital lamina of ethmoid bone (lamina papyricea) while the posterior part attaches into the orbital lamina horizontally.^[5]

  Innervation

  [edit]

  The ethmoidal air cells receive sensory innervation from the anterior and the posterior ethmoidal nerve (which are ultimately derived from the ophthalmic branch (CN V₁) of the trigeminal nerve (CN V)),^[3] and the orbital branches of the pterygopalatine ganglion, which carry the postganglionic parasympathetic nerve fibers for mucous secretion from the facial nerve.^{[clarification needed][citation needed]}

  Haller cells

  [edit]

  Haller cells are air cells situated beneath the ethmoid bulla along the roof of the maxillary sinus and the most inferior portion of the lamina papyracea, including air cells located within the ethmoid infundibulum.^[8] These may arise from the anterior or posterior ethmoidal sinuses.^{[citation needed]}

  Onodi cells

  [edit]

  Also known as a sphenoethmoidal air cell, an Onodi cell is a posterior ethmoidal air cell that lies superolateral to the sphenoid sinus, often extending into the anterior clinoid process.^[9] Onodi cells are clinically significant because they lie in close proximity to the optic nerve and internal carotid artery, so surgeons should be aware of their existence when performing surgery on the sphenoid sinus so as not to damage these important structures.

  A central Onodi air cell is a variation in which a posterior ethmoid cell lies superior to the sphenoid sinus in a midline position with at least one optic canal bulge.^[10]

  Ethmoid sinus
  Frontal view of paranasal sinuses
  Coronal section of nasal cavities.
  Details
  Nerve	Posterior ethmoidal nerve
  Identifiers
  Latin	cellulae ethmoidales, labyrinthi ethmoidales
  MeSH	D005005
  TA98	A06.1.03.005
  TA2	3180
  FMA	84115
  Anatomical terms of bone [edit on Wikidata]

The ethmoidal labyrinth or lateral mass of the ethmoid bone consists of a number of thin-walled cellular cavities, the ethmoid air cells, arranged in three groups, anterior, middle, and posterior, and interposed between two vertical plates of bone; the lateral plate forms part of the orbit, the medial plate forms part of the nasal cavity. In the disarticulated bone many of these cells are opened into, but when the bones are articulated, they are closed in at every part, except where they open into the nasal cavity.^[1]

Surfaces

[edit]

The upper surface of the labyrinth presents a number of half-broken cells, the walls of which are completed, in the articulated skull, by the edges of the ethmoidal notch of the frontal bone. Crossing this surface are two grooves, converted into two openings by articulation with the frontal; they are the anterior and posterior ethmoidal foramina, and open on the inner wall of the orbit. The posterior surface presents large irregular cellular cavities, which are closed in by articulation with the sphenoidal concha and orbital process of palatine bone. The lateral surface is formed of a thin, smooth, oblong plate, the lamina papyracea (os planum), which covers in the middle and posterior ethmoidal cells and forms a large part of the medial wall of the orbit; it articulates above with the orbital plate of the frontal bone, below with the maxilla and orbital process of the palatine, in front with the lacrimal, and behind with the sphenoid.^[1]

In front of the lamina papyracea are some broken air cells which are overlapped and completed by the lacrimal bone and the frontal process of the maxilla. A curved lamina, the uncinate process, projects downward and backward from this part of the labyrinth; it forms a small part of the medial wall of the maxillary sinus, and articulates with the ethmoidal process of the inferior nasal concha.^[1]

The medial surface of the labyrinth forms part of the lateral wall of the corresponding nasal cavity. It consists of a thin lamella, which descends from the under surface of the cribriform plate, and ends below in a free, convoluted margin, the middle nasal concha. It is rough, and marked above by numerous grooves, directed nearly vertically downward from the cribriform plate; they lodge branches of the olfactory nerves, which are distributed to the mucous membrane covering the superior nasal concha. The back part of the surface is subdivided by a narrow oblique fissure, the superior meatus of the nose, bounded above by a thin, curved plate, the superior nasal concha; the posterior ethmoidal cells open into this meatus. Below, and in front of the superior meatus, is the convex surface of the middle nasal concha; it extends along the whole length of the medial surface of the labyrinth, and its lower margin is free and thick. The lateral surface of the middle concha is concave, and assists in forming the middle meatus of the nose. The middle ethmoidal cells open into the central part of this meatus, and a sinuous passage, termed the infundibulum, extends upward and forward through the labyrinth and communicates with the anterior ethmoidal cells, and in about 50% of skulls is continued upward as the frontonasal duct into the frontal sinus.^[1]

n human anatomy, the neurocranium, also known as the braincase, brainpan, or brain-pan,^[1][2] is the upper and back part of the skull, which forms a protective case around the brain.^[3] In the human skull, the neurocranium includes the calvaria or skullcap. The remainder of the skull is the facial skeleton.

In comparative anatomy, neurocranium is sometimes used synonymously with endocranium or chondrocranium.^[4]

Structure

[edit]

The neurocranium is divided into two portions:

• the membranous part, consisting of flat bones, which surround the brain; and
• the cartilaginous part, or chondrocranium, which forms bones of the base of the skull.^[3]

In humans, the neurocranium is usually considered to include the following eight bones:

• 1 ethmoid bone
• 1 frontal bone^[5]
• 1 occipital bone
• 2 parietal bones
• 1 sphenoid bone
• 2 temporal bones

The ossicles (three on each side) are usually not included as bones of the neurocranium.^[6] There may variably also be extra sutural bones present.

Below the neurocranium is a complex of openings (foramina) and bones, including the foramen magnum which houses the neural spine. The auditory bullae, located in the same region, aid in hearing.^[7]

The size of the neurocranium is variable among mammals. The roof may contain ridges such as the temporal crests.

Development

[edit]

The neurocranium arises from paraxial mesoderm. There is also some contribution of ectomesenchyme. In Chondrichthyes and other cartilaginous vertebrates this portion of the cranium does not ossify; it is not replaced via endochondral ossification.