In most cases, the mechanism by which an excitatory neurotransmitter produces an e.p.s.p. in the postsynaptic cell is the same as that by which ACh depolarizes the muscle at the neuromuscular junction. That is, the transmitter opens channels in the postsynaptic membrane that are permeable to sodium and potassium ions. The altered balance of sodium and potassium permeability then depolarizes the postsynaptic cell, as described in Chapter 8. We saw in Chapter 5 that the membrane potential is controlled by the ratio of sodium to potassium permeability. Consequently, a depolarization might result from either an increase in sodium permeability or a decrease in potassium permeability. Indeed, at some synapses, the e.p.s.p. is produced by a reduction in postsynaptic potassium permeability. For instance, ACh produces a long-lasting depolarization of sympathetic ganglion neurons in the frog, caused by a decrease in the potassium permeability of the neuron. Acetylcholine closes a type of potassium channel in the neuron, so that outward potassium current declines and the resting inward sodium current exerts a greater influence on the membrane potential.
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