Which of the following best describes the relationship between graded potentials and distance

Graded potentials

Graded potentials are produced by stimuli opening a gated channel and are local potentials. They cannot spread over long distances away from the stimulation.

Sodium ions enter cells, attracted to negative charges on inner membrane surfaces. As positive charges move outward, membrane potential moves toward 0 mV. Depolarization is from any change between resting membrane potential to a less negative potential. Depolarization reveals changes in potential from −70 mV to lesser negative values (−65, −45, and −10 mV), and to membrane potentials above 0 mV (+10, +30 mV). For all of these, membrane potential becomes more positive.

As the plasma membrane depolarizes, the outer surface releases sodium ions. With other extracellular sodium ions, the ions move to open channels, and replace ions already in the cell. Local current describes movement of positive charges parallel to the inside and outside of the depolarizing membrane.

In graded potentials, the amount of depolarization is reduced over distance, away from the stimuli. Local current is greatly reduced, because cytoplasm has a large resistance to ion movement. Some sodium ions entering cells move out across the membrane, through sodium leak channels. At a far enough distance away from the point of entry, effects on membrane potential are not detectable. The greatest change in membrane potential is based on stimulus size, which determines how many sodium ion channels are open. With more open channels, larger amounts of sodium ions enter, more of the membrane is affected, and there is more depolarization.

Membrane potential soon returns to resting levels when the chemical stimulus is removed, and normal membrane permeability is restored. Repolarization is restoration of normal resting membrane potential after depolarization. Repolarization usually requires combinations of ion movement through membrane channels. Efflux of potassium is mostly responsible for repolarization, requiring ion pumps, mainly the sodium-potassium exchange pump. As a gated potassium ion channel opens from stimuli, effects are opposite. Potassium ion outflow increases. The inner part of the cell loses positive ions, becoming more negative. Hyperpolarization is due to the loss of positive ions. It is an increase in negativity of resting membrane potential, such as from −70 to −80 mv, or more. A local current distributes this effect to neighboring areas of the plasma membrane, and the effect decreases over distance from the open channels.

Graded potentials happen in membranes of epithelial cells, fat cells, nerve and muscle cells, gland cells, and sensory receptors. Potentials often begin various cell functions, such as when a graded potential at a gland cell surface initiates exocytosis of secretory vesicles. Another example is when a neuromuscular junction’s motor end plate is stimulated by a graded potential, due to ACh. This may trigger an action potential in nearby areas of the sarcolemma. While graded potentials are supported by the motor end plate, the rest of the sarcolemma has of excitable membrane. These areas are different because they have voltage-gated ion channels. When a graded potential causes hyperpolarization in a neuron, an action potential is not likely. If a graded potential causes depolarization, an action potential is more likely.

Threshold and the all-or-none principle [email protected]

An action potential is stimulated only when a graded potential depolarizes the axolemma to a specific level. The threshold is the membrane potential at which an action potential begins. An axon's threshold is usually between − 60 and − 55 mV. This corresponds to a depolarization of 10–15 mV. Any stimulus that changes resting membrane potential from − 70 to − 62 mV produces only a graded depolarization and not an action potential. When the stimulus is removed, the membrane potential returns to its resting level. Local currents are created by the graded depolarization of the axon hillock. They cause depolarization of the initial axon segment.

For excitable membranes, including axons, a graded depolarization is like pressure on a gun's trigger. The action potential is similar to that when the gun fires. Every stimulus bringing the membrane to threshold creates identical action potentials. As long as a stimulus exceeds threshold, the action potential is independent of the strength of the depolarizing stimulus. This is known as the all-or-none principle. It applies to all excitable membranes. The stimulus either triggers a typical action potential or none at all.

B Retinal Output Characteristics

Receptor cells influence the bipolar cells which in turn generate graded potentials and influence ganglion cell firing. What is the nature of the message the ganglion cells pass onto the brain? On the retina nearly 100 million receptor cells converge onto approximately 1 million ganglion cells so some type of data reduction must take place. Uniform illumination of the retina has very little effect on ganglion cell firing. Rather the ganglion cells prefer to respond to discrete stimulation such as small spots. The term used to define the area of the retina that when illuminated influences the activity of a single ganglion cell is the receptive field (Hartline, 1940).

A very simple experiment is done to analyze the receptive fields. A discrete light stimulus is shown on the eye, and the electrical activity from a single nerve fiber or ganglion cell is recorded (Fig. 10-15). How does the firing change when a small area of the retina is illuminated? Ganglion cells have a low spontaneous firing rate of about 5/second even in the dark, and their response to light is either to increase their firing rate or to decrease their firing rate. Small spots of light which illuminate certain parts of the retina have no effect whatsoever on the activity of certain ganglion cells. This light is outside their respective fields. However, once the light enters the receptive field of a cell, it has a marked effect.

Ganglion cell receptive fields have two key characteristics: (1) the receptive fields are circular with the ganglion cell in the geometrical center of its field and (2) the receptive fields are primarily of two types: the ON-center and the OFF-center.

Figure 10-16 shows the basic features of a ganglion cell's response to stimulation of its receptive field. Receptive fields of an ON-center type have a central region where a light coming on makes the cell increase its firing rate. The response to central illumination is inhibited if the surrounding region is illuminated at the same time. An annulus (ring) of light illuminating only the surround of the receptive field inhibits the spontaneous activity of the cell when it comes on and causes a burst of spikes when it goes off. This type of ganglion cell then has an ON-center and an opponent OFF-surround. Thus it signals with an increased rate of firing when the center is brighter than the average illumination of the surround.

The other main type of ganglion cell has exactly the opposite response to light, an OFF-center response. It gives an OFF-response to illumination of the center of its receptive field, and an ON-response to illumination of the surround. This class of cell signals when the center is darker than the average of the surround.

We can now see why these two types of large ganglion cells do not effectively transmit information about the absolute level of light intensity. They respond best to information about the local grading of light intensity. ON-center and OFF-center cells also have different temporal adaptation curves, and they can signal how recently the center became brighter than the surround. Thus ganglion cells respond very markedly to spatial and temporal changes in light intensity.

It is a fact that the properties of the retina enable us to detect local differences in light intensities in the presence of background illumination which can vary over the tremendous range of 1011. On the basis of cell discharge rate alone, the ganglion cells can signal over only a very limited dynamic range. The lowest useful rate in which they can signal is probably 1 spike/second while the highest (limited by the refractory period of the axons) is somewhat less than 1000 spikes/second. Thus the discharge frequently varies only over a range of 103, but we can detect differences over a range of 1011. This is because the ganglion cells are very sensitive to the local gradient of light intensity. However, ganglion cells do discharge within the same receptive field in relation to light intensity. The greater the light intensity, the faster the firing rate. The relationship between intensity and firing rate is roughly logarithmic.

The OFF-surround of the ON-center cell is sharpened by the actions of the horizontal cells. In Figure 10-11 a horizontal cell is shown between the receptor cells and the bipolar cells. Its processes course beneath the receptor cells and contact both the receptor and bipolar cells. Horizontal cells receive their input from the receptor cells and provide lateral inhibition to adjacent bipolar cells and receptor cells; they inhibit adjacent receptor and bipolar cell activity (Naka and Witkovsky, 1972). In some species horizontal cells do not possess an axon and appear to be electrically coupled. These cells provide one of the best illustrations of local circuit interactions (see Chapter 6). Potentials in one horizontal cell spread electrotonically to other horizontal cells so that they can influence a large area of the retina. Since the horizontal cells sum signals from a large area, they respond best to diffuse fields of light. In this way the horizontal cells provide lateral inhibition and sharpen contrast (Kaneko, 1971).

In monkey and man, ganglion cells are sensitive not only to differences in light intensity between center and surround but also to differences in the wavelength of the light. Some cells may respond ON to red in the center and OFF to green in the surround, or vice versa. They also may respond to other OFF and ON combinations with blue or white. Such cells transmit information both about color and about spatial changes.

The rich system of retinal circuitry is not yet understood in complete detail, and the nature of certain interactions still must be worked out. Also many more complicated types of ganglion cell receptor fields need to be studied in more detail (Drujan and Svaetichin, 1972). Some are direction sensitive, others are sensitive to motion, and yet others are sensitive to the size of a stimulus.

In summary, at the retina a form is analyzed in terms of receptive fields, a series of closely spaced dots and contours. The image is captured on the retina and converted into a changing pattern of ganglion cell activity by the neuronal circuitry of the retina. Differences in ganglion cell response depend mostly on differences in illumination. A steady background illumination is largely discarded information. The retina is extremely refined in detecting contrasts, such as an edge moving and crossing the opposing regions of a receptive field. As an edge moves into the surround, impulse activity in the ganglion cell slows, and as it hits the ON-center impulse activity becomes most vigorous.

Position on the retinal surface is place coded so that a ganglion cell fires in response to light in its receptive field. Thus an object (form) creates a mosaic of ganglion cell activity. Each cell sends the brain coded information about the nature of stimulation in its receptive field and the location of that receptive field in reference to others. The job of the brain then is to process this coded information, reassemble it, and translate it into something meaningful. The first processing station is the lateral geniculate nucleus.

Sensory receptors

Sensory receptors have specialized functions, and respond to environmental changes in stimuli. Usually, activation of these receptors by stimuli causes graded potentials triggering nerve impulses along the afferent PNS fibers reaching the CNS. Awareness of stimulus is called sensation, while interpretation of sensation is called perception. Chemoreceptors respond to chemicals in a solution, such as molecules that are tasted or smelled, or any changes in chemistries of blood or interstitial fluid. Mechanoreceptors react to mechanical forces, including BP, other types of pressure, touch, stretching, and vibrations. Nociceptors respond to damaging stimuli, resulting in pain, which include extreme cold or heat, excessive pressure, and inflammatory chemicals. Their signals stimulate subtypes of chemoreceptors, mechanoreceptors, and thermoreceptors. Photoreceptors react to light, including the receptors in the retinas of the eyes. Thermoreceptors respond to temperature changes.

The three classifications of sensory receptors are based on their location. Enteroceptors respond to stimuli from outside the body and are usually near or upon the body surface. They react to pressure, touch, pain, and temperature in the skin, and also include most receptors of the special senses (hearing, vision, equilibrium, smell, and taste). Interoceptors respond to stimuli inside the body, including from blood vessels and internal viscera. They are also called visceroceptors, monitoring chemical changes, temperature, and tissue stretching. They may cause discomfort, pain, hunger, or thirst, but are usually not perceived. Proprioceptors also respond to internal stimuli, with more restricted locations. They are within connective tissue coverings of bones and muscles, and skeletal muscles, joints, ligaments, and tendons. They inform the brain of movements by monitoring stretching that occurs in the organs in which they are contained.

Most sensory receptors are within the general senses. They are modified dendritic endings of sensory neurons, throughout the body, and monitor most general sensory information. Receptors for the special senses are in the complex sense organs. In the eyes, there are sensory neurons and nonneural cells forming the lens and supporting wall. There are also simple general sense receptors, involved in tactile sensation, mixing pressure, touch, stretching, and vibrations. They are also involved in temperature, pain, and proprioceptor “muscle sensing.” One type can respond to different stimuli. Different types can respond to similar stimuli.

General sensory receptors are nonencapsulated (free) or encapsulated. Nonencapsulated nerve endings are most common in the epithelia and connective tissues, responding mostly to temperature and painful stimuli, but also to tissue movement caused by pressure. Nerve endings responding to cold temperature are in the superficial dermis, while those responding to hot temperatures are deeper in the dermis. Tactile (Merkel) discs are in the deepest epidermis, acting as light touch receptors. Hair follicle receptors wrap around hair follicles, and are light touch receptors detecting hair bending.

All encapsulated nerve endings have one or more fiber terminals of sensory neurons in a connective tissue capsule. Most are mechanoreceptors, with variances in distribution, shape, and size. Tactile corpuscles (Meissner’s corpuscles) are just below the epidermis and are used for touch discrimination (see Fig. 1.18). Lamellar corpuscles (Pacinian corpuscles) are deep in the dermis and subcutaneous tissue, stimulated by deep pressure, and respond only when pressure is first applied (see Fig. 1.19). Bulbous corpuscles (Ruffini endings) in the dermis, subcutaneous tissue, and joint capsules react to deep, continuous pressure. Muscle spindles in the perimysium of each skeletal muscle detect muscle stretching, initiating a reflex that resists the stretch. Tendon organs are near the junctions of skeletal muscles and tendons, respond to stretching of tendon fibers, then reacting with a reflex that causes relaxation of the contracting muscle. Joint kinesthetic receptors monitor stretch in articular capsules around synovial joints, providing data on joint position and motion.

4 Nonspiking APL and DPM Neural Network

APL neurons, and probably DPM neurons also (Glenn C. Turner, personal communication), function as nonspiking neurons (Papadopoulou et al., 2011), which is a type of neuron that transmits signals via graded potential instead of action potential (Roberts and Bush, 1981). Graded potential does not rely on voltage-gated sodium channels to travel through the neuronal fibers, but instead on passive propagation, which is faster but raises a concern of spatial decrement in amplitude. These features make the nonspiking neuron a good candidate to integrate multiple input signals for downstream modulation along the wide-extending fibers. Indeed, APL and DPM neurons broadly innervate the MB lobes (Fig. 3.2), most likely making synapses with every KC, and respond to various odors as well as electric shock (Liu and Davis, 2009; Wu et al., 2011; Yu et al., 2005). It has been demonstrated that a single pair of the APL neuron is the Drosophila equivalent of a group of the honeybee GABAergic feedback neurons, receiving odor information from the MB lobes and releasing GABA inhibition to the MB calyx (Grünewald, 1999; Lin et al., 2014). In addition, by utilizing multiple types of neurotransmissions (Table 3.1) an APL and DPM neural network offers great versatility in downstream modulation, such as ASM stabilization, ARM consolidation, decision-making, sleep regulation (Haynes et al., 2015; P.-T. Lee et al., 2011; Wu et al., 2011, 2013, 2015).

Ciliary Photoreceptors

Photoreceptors of the distal retina function in a profoundly different way. Their resting potential is relatively depolarized (∼–35 mV) owing to a high resting gNa/gK ratio, and illumination produces a hyperpolarizing receptor potential graded with light intensity (Figure 8). The light sensitivity is significantly lower than in proximal photoreceptors, but the purpose here is not range fractionation (unlike rods and cones of the vertebrate retinas). Instead, ciliary photoreceptors play a fundamentally different role from that of their microvillar counterparts: the information output ultimately entails action potentials, which, of course, could not be caused by light-induced hyperpolarization. It is a reduction of illumination that causes firing in these axons: the effect of light is to remove, in a time- and intensity-dependent way, the steady-state inactivation of voltage-dependent calcium channels, such that when illumination is decreased (e.g., when an approaching predator casts a shadow on the animal's visual field), the return to a depolarized membrane potential triggers a Ca spike. As such, these cells function as dark detectors and activation of the phototransduction cascade serves the function of priming them to respond to light dimming.

1.2.3 Retinal structure

The different types of neuronal cells in the retinal layer include bipolar cells, ganglion cells, horizontal cells, retina amacrine cells, and rod and cone photoreceptors. Fig. 1.2 shows simply the structure of the vertebrate retina. Retinal structure includes photoreceptors as light sensors. A wide spectrum of light enters the eye and reaches the photoreceptors. These photoreceptors generate graded potentials, and bipolar cells transduce these graded potentials to the proper stimulation signals for triggering ganglion cells. In the dark condition, a photoreceptor (rod/cone) cell inhibits (hyperpolarizes) the ON bipolar cells, while it stimulates (depolarizes) the OFF bipolar cells by releasing glutamate. Under light conditions, the entering light produces graded potentials via the photoreceptor leading to hyperpolarization. On the other hand, retinal ganglion cells transmit visual information from the explained retina layer with propagation of action potentials through axons to several regions including the midbrain and diencephalon. These regions will process visual information at the end. One of the most important lessons of this part was that the position of neurons and their origin and the destination in the neural network provide valuable information about their functionality.

Damage to these cells as a result of aging and disease negatively affects vision and may even lead to blindness. One of the most important aspects of retinal prosthesis in recent decades has been the replacement of damaged photoreceptors with artificial photoreceptors. In recent years, researchers developed semiconductor-based interfaces for electrical transduction of light for retinal prosthesis application [1]. This semiconducting layer produces photoinduced potentials to trigger neurons. In Chapter 2, different types of neural interfaces embedded with semiconductor materials will be described. In brief, these interfaces upon light illumination can generate local photoinduced potentials or currents at their surfaces, which are the source of neural stimulation. Fig. 1.2B shows an animation that photoreceptors have been replaced by artificial semiconductor materials that absorb light in the visible spectrum. However, there are two different ways to implant the semiconductor interfaces: direct connection with the retina (epiretinal implant) or behind the retinal layer (subretinal).

F Conclusion and Summary

Neurons are highly sophisticated computational devices. For a single neuron, integration depends on the types of inputs impinging on it, the places where they arrive on the cell (dendrites versus soma), the geometry of the dendrites, the propagation characteristics of those dendrites (passive or active), and the highly individualized relation of the output signal to a specified level of depolarization. Output can be a pattern of action potentials, as in cells with axons, or a graded potential, as in amacrine neurons.

The importance of these graded interactions is that they greatly increase the functional capacity of the nervous system. It is still clear that the bulk of information processing appears through the classic sequence (action potentials, synaptic transmission, integration and action potentials), but local interactions appear to exert a subtle and vital influence and extend the integrative capacity of neurons. It was once thought that the nervous system operated in spite of these modulatory effects, but as more and more are discovered in relationship to specific functions and specific systems, it is clear that the nervous system uses them to gain the maximal capacities of its neurons and its informational processing capacities.

Is integration simply electrical as we have implicity assumed? Or is integration chemical as well? As we have witnessed in the previous chapter on synaptic transmission, each message causes a different set of ionic changes and in certain cases metabolic ones. Transmitters that are inhibitory, for example, bring the same basic message (inhibition) to the surface of the neuron, but they may be construed as lending a different affective state or diffuseness. Their time courses differ and, most significantly, the metabolic consequence of their action is unique. Dopamine alters cAMP levels in the cell; γ–aminobutyric acid, another transmitter, does not. If, then, the consequence is different and if this alters the affective state of the cell (its response to other inputs), then there must be another level of integration underlying the transient electrical one: a type of shifting, abiding pattern of neuronal metabolism. For example, some cells have rhythms and are more or less responsive depending on the part of the cycle in which they are functioning. In the pineal gland we have seen that neurotransmitter metabolism is cyclic as a result of the metabolic influence of its synaptic input. A neuron then is not simply excited, inhibited or modulated. It is affected by what came earlier (or what happens all at once) much like the corporate executive whose decision will sway one way or another depending on what he had for lunch, coffee or scotch. Neurons integrate in relation to their state which is set by certain of its inputs over its prior history.

There appear to be levels of integration: foreground integration and background integration. Foreground integration is up front using electrical signaling, and background integration is setting a metabolic temperament to these excitations. We shall now turn to an analysis of the organization of CNS transmitters.

A Brief Review of the Electrical Properties of Neurons

The electrical activity of a neuron is based on the relative concentration gradients and electrostatic gradients of ions within the cell and in the extracellular fluid, as well as the types of ion channels present within the neuron. The difference in charge between the intracellular and extracellular sides of the membrane creates an electrical potential, measured in units of volts (V). A neuron membrane at resting potential is about –70 mV. This is due to differences in the permeability of various inorganic ions, particularly sodium (Na+), potassium (K+), and chloride (Cl−), as well as to the active contributions of a sodium-potassium pump (Figure 4.1). Ions moving across the membrane generate a measurable current (I), the movement of charge over time. The movement of ions across the membrane is limited by the membrane resistance (R). This resistance is generated by properties of the membrane, such as how many channels are open or closed. The relationship among the membrane potential, the current flow, and the membrane resistance is described by Ohm’s law: V = I × R. This relationship is the fundamental basis of electrophysiological techniques.

Neurons communicate by causing changes in membrane potential in other neurons. For example, a neurotransmitter binding to a ligand-gated ion channel opens the channel to allow more ions to flow through the membrane. Relative to the membrane’s resting potential, this current flow can make the membrane potential more positive, an effect called depolarization. Alternatively, current flow can make the membrane potential more negative, an effect called hyperpolarization. Whether a depolarization or hyperpolarization effect occurs depends on the charge of the flowing ions. This local voltage change is called a graded potential or localized potential, and its magnitude is proportional to the strength of the stimulus. A local voltage change that makes the membrane potential more positive is called an excitatory postsynaptic potential (EPSP), while a local voltage change that makes the membrane potential more negative is called an inhibitory postsynaptic potential (IPSP). Different EPSP and IPSP events combine to form an overall signal in the postsynaptic neuron. These localized potentials can add up in space (called “spatial summation”) and time (called “temporal summation”). If enough localized potentials sum to depolarize the membrane to a threshold point, usually around –55 mV, an action potential will occur.

An action potential, also referred to as a spike, is an all-or-none, rapid, transient depolarization of the neuron’s membrane. A local depolarization to the threshold potential opens voltage-gated sodium channels, and the rapid influx of sodium ions brings the membrane potential to a positive value (Figure 4.2). The membrane potential is restored to its normal resting value by the delayed opening of voltage-gated potassium channels and by the closing of the sodium channels. A refractory period follows an action potential, corresponding to the period when the voltage-gated sodium channels are inactivated. The all-or-none generation of an action potential initiates a wave of depolarization that preserves the amplitude of the voltage change as it propagates down the axon’s membrane.

In a chemical synapse, depolarization stimulates the fusion of synaptic vesicles with the presynaptic membrane and the release of neurotransmitter molecules into the synaptic cleft. The neurotransmitters bind to receptor proteins associated with particular ion channels on the postsynaptic membrane. These ion channels then generate EPSP and IPSP events in the postsynaptic neuron, which can, in turn, sum to generate an action potential in that neuron.

Many more details on the electrical properties of neurons can be found elsewhere. What is important in the context of discussing electrophysiology methods is to understand that scientists can study these properties at many different levels of investigation. For example, an investigator may want to know the frequency of action potentials in a specific neuron over time to decipher how a neuron encodes a particular stimulus or action. This kind of experiment could be performed using an extracellular recording, either in vitro, or in an awake, behaving animal. Alternatively, an investigator may want to know how the presence of a drug in the extracellular fluid affects the ability of a specific ion channel to pass current. This experiment could be performed using a patch clamp technique in a heterologous expression system. Whether in the context of circuit analysis or the molecular basis of the membrane potential, nearly any aspect of neuronal physiology can be investigated with the electrophysiology methods described in detail later. Before we describe these methods, let’s examine the tools and equipment necessary to perform an electrophysiological recording.

Key Terms

Action potential:

A transient all-or-nothing change in the membrane potential which propagates along the axon like a wave. Action potentials, unlike electrotonic potentials, do not decay because they are self-regenerative.

Information is contained in a short-lived burst of action potentials.

A property of the membrane which allows charge to be stored and separated. It introduces a distortion in the time course of passively conducted signals. Without capacitance all changes in potentials would be instantaneous.

A unit of electrical charge. When 1 coulomb of charge flows for 1 second the quantity of current is called an ampere.

The rate of flow of charge. The unit of measure is the ampere.

Reduction of the membrane potential from resting value toward zero.

Localized, graded potentials that are determined by the passive electrical properties of cells. The measure of this passive decay is the space constant.

The potential at which, for the given ion gradient across the membrane, there is no net current flow. The relationship between a particular ionic gradient and its equilibrium potential is given by the Nernst equation.

Membranes which generate action potentials. Such membranes contain ionic channels whose permeability characteristics are voltage-dependent.

An increase in the membrane potential from its resting value.

Information that is contained in the structure of action potentials in a given cycle.

The plasma membrane of a glial cell wrapped many times around the axon. It serves to increase the metabolic efficiency of the nerve and increase the speed of action potential propagation.

The relationship between the concentration of ionic species which permeate the membrane and the membrane potential: E = 58 log ([X]o/[X]i), where Xi and Xo, respectively, are the internal and external ion concentrations.

Localized areas of the axon where myelin does not wrap the axon. Nodes occur at regular intervals.

Relates voltage V to current I and resistance R: V = IR.

The property of the membrane that allows ions to diffuse through it. Ions permeate through specific channels.

Information is contained in the time interval elapsing between two ongoing repetitive and rhythmic signals arriving at the same location.

A type of coding whereby information at one defined place is presented to another defined place along defined neuronal pathways.

A pore which allows K+ ions to pass through it but which excludes other ions not closely related (in size and charge) to potassium.

The time following each action potential during which a stimulus cannot initiate a second action potential.

The electrical potential across the plasma membrane of neurons or muscle cells in the quiescent state. The resting potential (approximately −70 mV in most neurons) results from a very slight excess of negative charge on the inside of the neuron. At rest the membrane is selectively permeable to potassium ions and the difference in potassium ion concentration (high inside, low outside) establishes a diffusion potential.

Conduction of action potentials along myelinated nerves whereby action potential currents leap from node to node.

Information is contained in the frequency of action potentials.

A pore which allows Na+ ions to pass through it but which excludes dissimilar ions. Excitable sodium channels in axons open and close in response to changes in membrane potential.

The enzyme located in membranes responsible for translocating sodium and potassium ions across the membrane against their ionic concentration gradients.

The distance over which a localized graded (electrotonic) potential decreases to l/e (377c) of its original size in an axon or muscle fiber. The value of the space constant is directly proportional to the square root of the fiber diameter.

Information is contained in changes in the probability of firing as a result of a stimulus. Such information is distributed widely over many fibers.

A type of general code whereby information is contained in the temporal pattern of action potentials.

A quaternary ammonium compound that selectively blocks potassium channels in neuronal and muscle membranes.

A poison which selectively blocks excitable sodium (regenerative) channels.

The value of the membrane potential or depolarization at which an action potential is initiated.

A technique for displacing the membrane potential to a defined value and holding it there while measuring the currents.