the hodgkin-huxley equations. these equations have been extensively modified by later research, but form the starting point for most theoretical studies of action potential biophysics. ion movement during an action potential.key: a) sodium (na+) ion. b) potassium (k+) ion. c) sodium channel. d) potassium channel. e) sodium-potassium pump. in the stages of an action potential, the permeability of the membrane of the neuron changes. at the resting state (1), sodium and potassium ions have limited ability to pass through the membrane, and the neuron has a net negative charge inside. once the action potential is triggered, the depolarization (2) of the neuron activates sodium channels, allowing sodium ions to pass through the cell membrane into the cell, resulting in a net positive charge in the neuron relative to the extracellular fluid. after the action potential peak is reached, the neuron begins repolarization (3), where the sodium channels close and potassium channels open, allowing potassium ions to cross the membrane into the extracellular fluid, returning the membrane potential to a negative value. finally, there is a refractory period (4), during which the voltage-dependent ion channels are inactivated while the na+ and k+ ions return to their resting state distributions across the membrane (1), and the neuron is ready to repeat the process for the next action potential. as the membrane potential is increased, sodium ion channels open, allowing the entry of sodium ions into the cell. this is followed by the opening of potassium ion channels that permit the exit of potassium ions from the cell. the inward flow of sodium ions increases the concentration of positively charged cations in the cell and causes depolarization, where the potential of the cell is higher than the cell's resting potential. the sodium channels close at the peak of the action potential, while potassium continues to leave the cell. the efflux of potassium ions decreases the membrane potential or hyperpolarizes the cell. for small voltage increases from rest, the potassium current exceeds the sodium current and the voltage returns to its normal resting value, typically −70 mv. however, if the voltage increases past a critical threshold, typically 15 mv higher than the resting value, the sodium current dominates. this results in a runaway condition whereby the positive feedback from the sodium current activates even more sodium channels. thus, the cell fires, producing an action potential. the frequency at which a neuron elicits action potentials is often referred to as a firing rate or neural firing rate. currents produced by the opening of voltage-gated channels in the course of an action potential are typically significantly larger than the initial stimulating current. thus, the amplitude, duration, and shape of the action potential are determined largely by the properties of the excitable membrane and not the amplitude or duration of the stimulus. this all-or-nothing property of the action potential sets it apart from graded potentials such as receptor potentials, electrotonic potentials, subthreshold membrane potential oscillations, and synaptic potentials, which scale with the magnitude of the stimulus. a variety of action potential types exist in many cell types and cell compartments as determined by the types of voltage-gated channels, leak channels, channel distributions, ionic concentrations, membrane capacitance, temperature, and other factors. the principal ions involved in an action potential are sodium and potassium cations; sodium ions enter the cell, and potassium ions leave, restoring equilibrium. relatively few ions need to cross the membrane for the membrane voltage to change drastically. the ions exchanged during an action potential, therefore, make a negligible change in the interior and exterior ionic concentrations. the few ions that do cross are pumped out again by the continuous action of the sodium–potassium pump, which, with other ion transporters, maintains the normal ratio of ion concentrations across the membrane. calcium cations and chloride anions are involved in a few types of action potentials, such as the cardiac action potential and the action potential in the single-cell alga acetabularia, respectively. although action potentials are generated locally on patches of excitable membrane, the resulting currents can trigger action potentials on neighboring stretches of membrane, precipitating a domino-like propagation. in contrast to passive spread of electric potentials (electrotonic potential), action potentials are generated anew along excitable stretches of membrane and propagate without decay. myelinated sections of axons are not excitable and do not produce action potentials and the signal is propagated passively as electrotonic potential. regularly spaced unmyelinated patches, called the nodes of ranvier, generate action potentials to boost the signal. known as saltatory conduction, this type of signal propagation provides a favorable tradeoff of signal velocity and axon diameter. depolarization of axon terminals, in general, triggers the release of neurotransmitter into the synaptic cleft. in addition, backpropagating action potentials have been recorded in the dendrites of pyramidal neurons, which are ubiquitous in the neocortex. these are thought to have a role in spike-timing-dependent plasticity. in the hodgkin–huxley membrane capacitance model, the speed of transmission of an action potential was undefined and it was assumed that adjacent areas became depolarized due to released ion interference with neighbouring channels. measurements of ion diffusion and radii have since shown this not to be possible. moreover, contradictory measurements of entropy changes and timing disputed the capacitance model as acting alone. alternatively, gilbert ling's adsorption hypothesis, posits that the membrane potential and action potential of a living cell is due to the adsorption of mobile ions onto adsorption sites of cells. maturation of the electrical properties of the action potential a neuron's ability to generate and propagate an action potential changes during development. how much the membrane potential of a neuron changes as the result of a current impulse is a function of the membrane input resistance. as a cell grows, more channels are added to the membrane, causing a decrease in input resistance. a mature neuron also undergoes shorter changes in membrane potential in response to synaptic currents. neurons from a ferret lateral geniculate nucleus have a longer time constant and larger voltage deflection at p0 than they do at p30. one consequence of the decreasing action potential duration is that the fidelity of the signal can be preserved in response to high frequency stimulation. immature neurons are more prone to synaptic depression than potentiation after high frequency stimulation. in the early development of many organisms, the action potential is actually initially carried by calcium current rather than sodium current. the opening and closing kinetics of calcium channels during development are slower than those of the voltage-gated sodium channels that will carry the action potential in the mature neurons. the longer opening times for the calcium channels can lead to action potentials that are considerably slower than those of mature neurons. xenopus neurons initially have action potentials that take 60–90 ms. during development, this time decreases to 1 ms. there are two reasons for this drastic decrease. first, the inward current becomes primarily carried by sodium channels. second, the delayed rectifier, a potassium channel current, increases to 3.5 times its initial strength. in order for the transition from a calcium-dependent action potential to a sodium-dependent action potential to proceed new channels must be added to the membrane. if xenopus neurons are grown in an environment with rna synthesis or protein synthesis inhibitors that transition is prevented. even the electrical activity of the cell itself may play a role in channel expression. if action potentials in xenopus myocytes are blocked, the typical increase in sodium and potassium current density is prevented or delayed. this maturation of electrical properties is seen across species. xenopus sodium and potassium currents increase drastically after a neuron goes through its final phase of mitosis. the sodium current density of rat cortical neurons increases by 600% within the first two postnatal weeks. neurotransmission anatomy of a neuron structure of a typical neuron neuron dendrite soma axon nucleus node ofranvier axon terminal schwann cell myelin sheath several types of cells support an action potential, such as plant cells, muscle cells, and the specialized cells of the heart (in which occurs the cardiac action potential). however, the main excitable cell is the neuron, which also has the simplest mechanism for the action potential. neurons are electrically excitable cells composed, in general, of one or more dendrites, a single soma, a single axon and one or more axon terminals. dendrites are cellular projections whose primary function is to receive synaptic signals. their protrusions, known as dendritic spines, are designed to capture the neurotransmitters released by the presynaptic neuron. they have a high concentration of ligand-gated ion channels. these spines have a thin neck connecting a bulbous protrusion to the dendrite. this ensures that changes occurring inside the spine are less likely to affect the neighboring spines. the dendritic spine can, with rare exception (see ltp), act as an independent unit. the dendrites extend from the soma, which houses the nucleus, and many of the "normal" eukaryotic organelles. unlike the spines, the surface of the soma is populated by voltage activated ion channels. these channels help transmit the signals generated by the dendrites. emerging out from the soma is the axon hillock. this region is characterized by having a very high concentration of voltage-activated sodium channels. in general, it is considered to be the spike initiation zone for action potentials, i.e. the trigger zone. multiple signals generated at the spines, and transmitted by the soma all converge here. immediately after the axon hillock is the axon. this is a thin tubular protrusion traveling away from the soma. the axon is insulated by a myelin sheath. myelin is composed of either schwann cells (in the peripheral nervous system) or oligodendrocytes (in the central nervous system), both of which are types of glial cells. although glial cells are not involved with the transmission of electrical signals, they communicate and provide important biochemical support to neurons. to be specific, myelin wraps multiple times around the axonal segment, forming a thick fatty layer that prevents ions from entering or escaping the axon. this insulation prevents significant signal decay as well as ensuring faster signal speed. this insulation, however, has the restriction that no channels can be present on the surface of the axon. there are, therefore, regularly spaced patches of membrane, which have no insulation. these nodes of ranvier can be considered to be "mini axon hillocks", as their purpose is to boost the signal in order to prevent significant signal decay. at the furthest end, the axon loses its insulation and begins to branch into several axon terminals. these presynaptic terminals, or synaptic boutons, are a specialized area within the axon of the presynaptic cell that contains neurotransmitters enclosed in small membrane-bound spheres called synaptic vesicles. initiation before considering the propagation of action potentials along axons and their termination at the synaptic knobs, it is helpful to consider the methods by which action potentials can be initiated at the axon hillock. the basic requirement is that the membrane voltage at the hillock be raised above the threshold for firing. there are several ways in which this depolarization can occur. when an action potential arrives at the end of the pre-synaptic axon (top), it causes the release of neurotransmitter molecules that open ion channels in the post-synaptic neuron (bottom). the combined excitatory and inhibitory postsynaptic potentials of such inputs can begin a new action potential in the post-synaptic neuron. dynamics action potentials are most commonly initiated by excitatory postsynaptic potentials from a presynaptic neuron. typically, neurotransmitter molecules are released by the presynaptic neuron. these neurotransmitters then bind to receptors on the postsynaptic cell. this binding opens various types of ion channels. this opening has the further effect of changing the local permeability of the cell membrane and, thus, the membrane potential. if the binding increases the voltage (depolarizes the membrane), the synapse is excitatory. if, however, the binding decreases the voltage (hyperpolarizes the membrane), it is inhibitory. whether the voltage is increased or decreased, the change propagates passively to nearby regions of the membrane (as described by the cable equation and its refinements). typically, the voltage stimulus decays exponentially with the distance from the synapse and with time from the binding of the neurotransmitter. some fraction of an excitatory voltage may reach the axon hillock and may (in rare cases) depolarize the membrane enough to provoke a new action potential. more typically, the excitatory