Nerve cell action potential

Neurotransmitters affect receptors in two basic ways. Some bind to receptors which are said to have ionic effects. These receptors, when activated, operate to open tiny pores (ion-channels), allowing electrically charged particles (ions) to enter the nerve cell. When numerous ionic receptors are activated, this can result in either an excitation of the nerve cell (action potential) or, conversely, a calming of the nerve cell (hyperpolarization, which makes it less likely that the cell will fire). Excitation or inhibition depends on which specific type of channel is activated. This phenomenon is responsible for eliciting immediate and transient changes in neuronal excitability (for example, this occurs when a motor neuron is activated and there is corresponding activation of a muscle, or when sensory events are perceived). 

Except in certain minor details, the action potentials of vertebrate skeletal muscle resemble those of nerve cells. Action potentials of cardiac muscle or barnacle muscle, however, differ in certain respects from those of nerve and skeletal muscle. The most striking feature of the action potential in the ventricle of the heart is its long duration (see Figure 39), lasting up to 1 sec in amphibians. The upstroke of these action potentials is due primarily to inward current... 

The Na" channel has a receptor site for cyclic GMP when cyclic GMP is bound, the channel is closed. This leads to a decrease in the intracellular Na ion concentration, resulting in hyperpolarisation of the cell membrane. This decreases the release of the neurotransmitter glutamate into the synapse that connects the photoreceptor cell to the bipolar neurones. In this specific case, a decrease in the neurotransmitter concentration in the synapse is a signal that results in depolarisation of the bipolar cell. The action potential in the bipolar cells communicate with ganglion cells, the axons of which form the optic nerve. Thus action potentials are generated in the axons which are... 

Conduction velocity of an action potential can be increased dramatically by the presence of myelin, a fatty sheath that surrounds the axon and that is interrupted into gaps every millimeter or so at the nodes of Ranvier. Myelin is elaborated by Schwann cells in the peripheral nervous system and by oligodendrocytes in the central nervous system (the biochemistry of myelin will be discussed later in the article). The presence of myelin will dramatically alter the mode and velocity of conduction of the action potential in the axon. As in unmyelinated nerves, the action potential is still transmitted from one section of the axon to another by the presence of local circuit currents. However, the fatty sheath of myelin has poor conduction properties and therefore acts as an insulator. Hence, the local circuit currents jump from one gap to another at the nodes of Ranvier and the rate of conduction is enhanced as local circuit currents travel faster than the action potential itself This process of discontinuous conduction is known as saltatory conduction. Numerous diseases involving myelin deficiency have been described clinically. As one might predict, demyelinating diseases have profound effects on neuronal conduction and on the well-being of the patient. A few of these conditions will be described briefly in the upcoming section on myelin biochemistry. 

The role of membrane transport and action potential is very important in the development of self-excited potential (as discussed in Chapter 11) and nerve transmission. For nerve excitation, action potentials play the key role. In the resting state, the polarized or resting muscle cell having a negative surface charge can be represented as in Fig. 15.3(a). When the negative ions migrate to the outer surface of the cell, it is activated or depolarized as indicated in Fig. 15.3(b) and the process is termed depolarization. ... 

Long nerve-cell process transmitting the action potential and ending as the synapse. 

Excitability refers to the capacity of nerves and other tissues (e.g. cardiac), as well as individual cells, to generate and sometimes propagate action potentials, signals that serve to control intracellular processes, such as muscle contraction or hormone secretion, and to allow for long- and short-distance communication within the organism. Examples of excitable cells and tissues include neurons, muscle and endocrine tissues. Examples of nonexcitable cells and tissues include blood cells, most epithelial and connective tissues. 

Voluntary muscle contraction is initiated in the brain-eliciting action potentials which are transmitted via motor nerves to the neuromuscular junction where acetylcholine is released causing a depolarization of the muscle cell membrane. An action potential is formed which is spread over the surface membrane and into the transverse (T) tubular system. The action potential in the T-tubular system triggers Ca " release from the sarcoplasmic reticulum (SR) into the myoplasm where Ca " binds to troponin C and activates actin. This results in crossbridge formation between actin and myosin and muscle contraction. 

The membranes of nerve cells contain well-studied ion channels that are responsible for the action potentials generated across the membrane. The activity of some of these channels is controlled by neurotransmitters hence, channel activity can be regulated. One ion can regulate the activity of the channel of another ion. For example, a decrease of Ca + concentration in the extracellular fluid increases membrane permeability and increases the diffusion of Na+. This depolarizes the membrane and triggers nerve discharge, which may explain the numbness, tinghng, and muscle cramps symptomatic of a low level of plasma Ca. ... 

Tamplin et. al. (54) observed that V. cholerae and A. hydrophila cell extracts contained substances with TTX-like biological activity in tissue culture assay, counteracting the lethal effect of veratridine on ouabain-treated mouse neuroblastoma cells. Concentrations of TTX-like activity ranged from 5 to 100 ng/L of culture when compared to standard TTX. The same bacterial extracts also displaced radiolabelled STX from rat brain membrane sodium channel receptors and inhibited the compound action potential of frog sciatic nerve. However, the same extracts did not show TTX-like blocking events of sodium current when applied to rat sarcolemmal sodium channels in planar lipid bilayers. 

In squid giant axons, PbTx causes a depolarization of the plasma membrane, repetitive discharges followed by depression of action potentials, and a complete blockade of excitability. This action is antagonized by TTX (83,84). PbTx depolarizes nerve terminals and induces neurotransmitter release (85,86) it depolarizes skeletal muscle cells (87) and increases the frequency of action potentials in crayfish nerve cord (88). PbTx also produces a contraction of the guinea pig ileum (89). All these effects are prevented by TTX. 

The K+ channels responsible for action potential repolarisation close fairly soon after repolarisation (usually within 5-10 ms). However, most nerve cells possess other K+ channels which are opened during nerve cell discharges but which stay open much longer. These do not contribute much to the repolarisation of individual action potentials but instead affect the excitability of the neuron over periods of hundreds of milliseconds or even seconds. 

As discussed previously, the neurohypophysis has a direct anatomical connection to the hypothalamus. Therefore, the hypothalamus regulates the release of hormones from the neurohypophysis by way of neuronal signals. Action potentials generated by the neurosecretory cells originating in the hypothalamus are transmitted down the neuronal axons to the nerve terminals in the neurohypophysis and stimulate the release of the hormones into the blood. The tracts formed by these axons are referred to as hypothalamic-hypophyseal tracts (see Figure 10.2). The action potentials are initiated by various forms of sensory input to the hypothalamus. Specific forms of sensory input that regulate the release of ADH and oxytocin are described in subsequent sections in this chapter. 

Action potential, or nerve impulse The wave of electrical activity that passes from the dendrites of the neuronal cell body, down the axon to the synaptic bouton. 

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