The released acetylcholine binds to acetylcholine receptors in the muscle cell plasma membrane, transiently opening the cation channels associated with them. The resulting influx of Na+ causes a local membrane depolarization.
3.
The local depolarization opens voltage-gated Na+ channels in this membrane, allowing more Na+ to enter, which further depolarizes the membrane. This, in turn, opens neighboring voltage-gated Na+ channels and results in a self-propagating depolarization (an action potential) that spreads to involve the entire plasma membrane (see Figure 11–31).
4.
The generalized depolarization of the muscle cell plasma membrane activates voltage-gated Ca2+ channels in the transverse tubules (T tubules— discussed in Chapter 16) of this membrane.
5.
This in turn causes Ca2+-release channels in an adjacent region of the sarcoplasmic reticulum (SR) membrane to open transiently and release Ca2+ stored in the SR into the cytosol. The T-tubule and SR membranes are closely apposed with the two types of channel joined together in a specialized structure, in which activation of the voltage-sensitive Ca2+ channel in the T-tubule plasma membrane causes a channel conformational change that is mechanically transmitted to the Ca2+-release channel in the SR membrane, opening it and allowing Ca2+ to flow from the SR lumen into the cytoplasm (see Figure 16–35). The sudden increase in the cytosolic Ca2+ concentration causes the myofibrils in the muscle cell to contract.
Whereas the initiation of muscle contraction by a motor neuron is complex, an even more sophisticated interplay of ion channels is required for a neuron to integrate a large number of input signals at its synapses and compute an appropriate output, as we now discuss.
In the central nervous system, a single neuron can receive inputs from thousands of other neurons, and it can in turn form synapses with many thousands of other cells. Several thousand nerve terminals, for example, make synapses on an average motor neuron in the spinal cord, almost completely covering its cell body and dendrites (Figure 11–40). Some of these synapses transmit signals from the brain or spinal cord; others bring sensory information from muscles or from the skin. The motor neuron must combine the information received from all these sources and react, either by firing action potentials along its axon or by remaining quiet.
Of the many synapses on a neuron, some tend to excite it, while others inhibit it. Neurotransmitter released at an excitatory synapse causes a small depolarization in the postsynaptic membrane called an excitatory postsynaptic potential (excitatory PSP), whereas neurotransmitter released at an inhibitory synapse generally causes a small hyperpolarization called an inhibitory PSP. The plasma membrane of the dendrites and cell body of most neurons contains a relatively low density of voltage-gated Na+ channels, and so an individual excitatory PSP is generally too small to trigger an action potential. Instead, each incoming signal initiates a local PSP, which decreases with distance from the site of the synapse. If signals arrive simultaneously at several synapses in the same region of the dendritic tree, the total PSP in that neighborhood will be roughly the sum of the individual PSPs, with inhibitory PSPs making a negative contribution to the total. The PSPs from each neighborhood spread passively and converge on the cell body. For long-distance transmission, the combined magnitude of the PSP is then translated, or encoded, into the frequency of firing of action potentials: the greater the stimulation (depolarization), the higher the frequency of action potentials.
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Neuronal Computation Requires a Combination of at Least Three Kinds of K+ Channels