The Resting Membrane Potential Can Be Changed by Synaptic Signals from a Presynaptic Cell

Although most cells of the body have a resting membrane potential, neurons and muscle cells are unique in that their membrane potential can be altered by a synaptic signal from another cell.

If a chemical synaptic transmission leads to a postsynaptic potential that is more positive in comparison with the resting level (e.g., from -75 to -65 mV), this is said to be an excitatory postsynaptic potential (EPSP) (Figure 4-3, A). It is called “excitatory” because each such synaptic transmission increases the chances that an action potential will originate at the initial segment of the postsynaptic cell’s axon. When an EPSP changes the postsynaptic membrane potential to a more positive value, the membrane is said to be depolarized. Depolarization of the postsynaptic membrane can result if the interaction of the chemical transmitter and its appropriate receptor on the post­synaptic membrane cause (ligand-gated) Na' channels to open. This allows Naⁱ ions to diffuse into the neuron as they begin to flow toward equilibrium across the membrane, moving the membrane potential toward the more positive sodium equilibrium potential. The ion channels that usually change their conductivity as a result of neurotransmitter binding with a receptor are the ligand-gated or chemically gated ion chan­nels (see Chapter 1).

Because the chemical transmitter is quickly removed from the synapse, the postsynaptic potential change is transient, lasting only a few milliseconds. Furthermore, because the change in ion flow resulting from receptor activation is limited, the magnitude of a postsynaptic potential is often quite small (e.g., 2-3 mV). However, it is greatest at the synapse. Although the depolarization spreads over the postsynaptic membrane, it decreases with the distance from the originating synapse, much as the waves created by throwing a stone into a lake decrease in size with the distance from where the stone fell.

If instead the presynaptic neurotransmitter’s interaction with the postsynaptic receptor results in opening of the mem­brane’s chemically gated K* channels, then K⁺ ions diffuse out, moving the membrane potential even closer to the equilib­rium potential for K⁺ (-90 mV). This change from the resting potential to a more negative membrane potential is called hyperpolarization. Such hyperpolarization of the postsynaptic membrane is called an inhibitory postsynapticpotential (IPSP) (Figure 4-3, B), because each such transmission makes it less likely that an action potential will result at the axon’s initial segment. As with EPSPs, IPSPs spread over the neuron’s mem­brane, and the hyperpolarization decreases with the distance from the originating synapse.