Final answer:
If chemically gated sodium channels in the postsynaptic membrane were completely blocked, smaller action potentials would result in the postsynaptic neuron because the blockade would prevent Na+ ions from entering the cell and causing necessary depolarization for a significant excitatory postsynaptic potential (EPSP).
Step-by-step explanation:
If the chemically gated sodium channels in the postsynaptic membrane were completely blocked, the most direct effect would be smaller action potentials resulting within the postsynaptic neuron. Normally, neurotransmitters such as acetylcholine bind to these channels, causing them to open and allowing Na+ ions to enter the postsynaptic cell. This influx of Na+ ions causes the membrane to depolarize, generating an excitatory postsynaptic potential (EPSP), which increases the likelihood of the postsynaptic neuron firing an action potential.
However, if these sodium channels are blocked, Na+ ions cannot enter the cell, which would prevent the necessary depolarization for creating a substantial postsynaptic potential. This decreased depolarization leads to reduced excitability of the neuron and therefore yields smaller action potentials or might even prevent action potentials from occurring, depending on the extent of the blockage.
It is important to note that neurotransmitter release would not stop, as it is initiated in the presynaptic neuron by calcium entry via voltage-gated calcium channels following an action potential. The options mentioning stopping of neurotransmitter release, the presynaptic membrane being unable to reach threshold, and the presynaptic neuron releasing a different neurotransmitter are incorrect as they are related to events before the synaptic cleft, not the action of the neurotransmitter on the postsynaptic membrane.