ionotropic GABA receptors allows CI to flow from outside the cell
(where Cl is more highly concentrated) to inside the cell. This pro-
duces a change in the membrane voltage such that the inside of the
cell becomes more negative, a hyperpolarization. The membrane
potential moves further away from the threshold for triggering the
opening of voltage-gated Na* channels and the resulting generation of
an action potential and neural signal. This is inhibition.
If the membrane voltage is measured in a postsynaptic cell as it re-
ceives excitatory input, depolarization of the membrane is observed.
This change in membrane potential—most often by way of ionotropic
glutamate receptors—is called an excitatory postsynaptic potential,
or EPSP. If excitatory signals are received repeatedly in close temporal
sequence from an input neuron, or are received from several different
input neurons at around the same time, then the depolarizing effects
on membrane voltage will be enhanced by the summed effects from
the individual EPSPs.
Similarly, if the membrane voltage is measured in a postsynaptic
cell as it receives inhibitory input, hyperpolarization of the membrane
is observed. This change in membrane potential—most often by way
of ionotropic GABA receptors—is called an inhibitory postsynaptic
potential, or IPSP. Just as with the summation of EPSPs, if inhibitory
signals are received repeatedly in close temporal sequence from an
input neuron, or are received from several different input neurons at
around the same time, then the hyperpolarizing effects on membrane
voltage will be enhanced by the summed effects from the individual