Final answer:
When neurotransmitter binding opens transmitter-gated ion channels on the postsynaptic membrane, it alters the ion permeability and may depolarize or hyperpolarize the postsynaptic membrane, leading to either an excitatory or inhibitory postsynaptic potential.
Step-by-step explanation:
When transmitter-gated ion channels in the membrane of a postsynaptic cell open in response to neurotransmitter binding, the primary consequence is an alteration in the ion permeability of the postsynaptic membrane. This change may indeed depolarize the postsynaptic membrane, leading to an excitatory or inhibitory postsynaptic potential depending on the type of ion channel that is opened and the specific ions that pass through. For instance, the binding of acetylcholine can open sodium channels, resulting in an influx of Na+ and a subsequent depolarization, potentially leading to an action potential if the threshold is reached. Conversely, the neurotransmitter GABA may trigger the opening of chloride channels, resulting in an influx of Cl- and hyperpolarization of the postsynaptic membrane, making it less likely to fire an action potential.