Final answer:
Increased trans-epithelial Na+ transport at a neuromuscular junction could lead to heightened synaptic activity and muscle contraction by causing more significant depolarization and more robust action potential generation.
Step-by-step explanation:
If trans-epithelial Na+ transport were to increase at the synapse in a neuromuscular junction, there would be a significant impact on synaptic transmission and muscle contraction. At the presynaptic membrane, an increase in Na+ entrance could lead to an enhanced depolarization, promoting more frequent or robust action potentials. This could result in a greater release of acetylcholine, the neurotransmitter at neuromuscular junctions. At the postsynaptic membrane, an increase in Na+ transport could lead to a stronger excitatory postsynaptic potential (EPSP). Higher levels of Na+ entering the muscle cell would cause more profound depolarization, potentially resulting in more forceful or sustained muscle contractions as more action potentials are triggered in muscle fibers.
The role of gated ion channels is crucial in this process. Once neurotransmitter, such as acetylcholine, binds to its receptor at the motor end plate, it causes the Na+ channels to open. Enhanced Na+ movement across the post-synaptic membrane can cause a significant local depolarization, possibly leading to an action potential that results in muscle contraction. The Ca2+ ions play a critical part in neurotransmitter release at the presynaptic membrane, while the action potential in muscle contraction is propagated by the Na+/K+ pump restoring the membrane potential.