| Action potentials are caused by changes in ion flows across cell membranes
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| The signal carried by a nerve cell reflects an abrupt change in the voltage potential difference across the cell membrane. The normal resting potential difference is a few millivolts, with the inside of the cell being negative, and is caused by an imbalance
of ions across the plasma membrane: the concentration of K+ ions is much greater inside cells than outside, whereas the opposite is true for Na+ ions. This difference is maintained by the action of the Na+/K+-ATPase (see Chapter 39). Only those ions to which the membrane is permeable can affect the potential, as they can come to an electrochemical steady state under the combined influence of concentration and voltage differences. Because the membrane in all resting cells is comparatively permeable to K+ as a result of the presence of voltage-independent (leakage) K+ channels, this ion largely controls the resting potential.
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| A change in voltage which tends to drive this resting potential towards zero from the normal negative voltage is known as a depolarization, whereas a process that increases the negative potential is called hyperpolarizing
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| Figure 40.2 Generation of action potential. Action potential is formed as follows. At the start of an action potential, the membrane is at its resting potential of about -70 mV; this is maintained by voltage-independent K+ channels. When an impulse is initiated by a signal from a neurotransmitter, voltage-dependent Na+ channels open. These allow inflow of Na+ ions, which alter the membrane potential to positive values. The Na+ channels then close, and K+ channels, called delayed rectifier channels, open to restore the initial balance of ions and the negative membrane potential. |
| So far, this picture is common to all cells. However, nerve cells contain voltage-dependent sodium channels that open very rapidly when a depolarizing change in voltage is applied. When they open, they allow the inward passage of huge numbers of Na+ ions from the extracellular fluid (Fig. 40.2), which swamps the resting voltage and drives the membrane potential to positive values. This reversal of voltage is the
action potential. Almost immediately afterwards, the sodium channels close and so-called delayed potassium channels open. These restore the normal resting balance of ions across the membrane and, after a short refractory period, the cell can conduct another action potential. Meanwhile, the action potential has spread by electrical conductance to the next segment of nerve membrane, and the entire cycle starts again.
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| Neurotransmitters alter the activity of various ion channels to cause changes in the membrane potential
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| Excitatory neurotransmitters cause a depolarizing change in voltage, in which case an action potential is more likely to occur. In contrast, inhibitory transmitters hyperpolarize the membrane, and an action potential is then less likely to occur.
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| Neurotransmitters act at synapses
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| Figure 40.3 Release of neurotransmitters. Neurotransmitters are released from vesicles at the synaptic membrane. (A) In the resting state, vesicles are attached to microtubules. (B) When an action potential is received, calcium channels open. (C) Vesicles move to the plasma membrane, and (D) bind to a complex of docking proteins. (E) Neurotransmitter is released, and (F) vesicles are recycled. |
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| Neurotransmitters are released into the space between cells at a specialized area known as a synapse (Fig. 40.3). In the
simplest case, they diffuse from the presynaptic membrane, across the synaptic space or cleft, and bind to receptors at the postsynaptic membrane. However, many neurons, particularly those containing amines, have several varicosities along the axon, containing transmitter. These varicosities may not be close to any neighboring cell, so transmitter released from them has the possibility of affecting many neurons. Nerves innervating smooth muscle are commonly of this kind.
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| When the action potential arrives at the end of the axon, the change in voltage opens calcium channels. Calcium entry is essential for mobilization of vesicles containing transmitter, and for their eventual fusion with the synaptic membrane and release through it.
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| Because transmitters are released from vesicles, impulses arrive at the postsynaptic cell in individual packets, or quanta. At the neuromuscular junction between nerves and skeletal muscle cells, a large number of vesicles are discharged at a time, and a single impulse may therefore be enough to stimulate contraction of the muscle cell. The number of vesicles released at synapses between neurons, however, is much smaller; consequently, the recipient cell will be stimulated only if the total algebraic sum of the various positive and negative stimuli exceeds its threshold. As each cell in the brain receives input from a huge number of neurons, this implies that there is a far greater capability for the fine control of responses in the central nervous system (CNS) than there is at the neuromuscular junction.
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