Final answer:
Serotonin contributes to synaptic plasticity through mechanisms that lead to either long-term potentiation or long-term depression at the sensory-motor synapse. These processes involve increasing or decreasing synaptic strength via the regulation of AMPA receptor presence on the postsynaptic membrane, which is modulated by calcium-dependent signaling pathways.
Step-by-step explanation:
Serotonin's influence on long-term changes at the sensory-motor synapse involves its role in synaptic plasticity, contributing to both long-term potentiation (LTP) and long-term depression (LTD). Serotonin (5-HT) can modulate the activity of other neurotransmitters and second messengers, which are critical for memory formation and neural plasticity. The cellular mechanisms behind LTP typically involve an increase in synaptic strength through the insertion of more AMPA receptors into the postsynaptic membrane. Conversely, LTD, which is essential for the pruning and weakening of synaptic connections, involves the removal of AMPA receptors from the postsynaptic membrane.
These changes are regulated by different intracellular pathways activated by the influx of calcium through NMDA receptors. In the case of LTP, repeated synaptic stimulation leads to a cascade that involves a calcium- and CaMKII-dependent pathway. For LTD, calcium initiates a different signaling cascade involving calcineurin and protein phosphatase 1, which ultimately leads to the endocytosis of AMPA receptors, thus rendering the postsynaptic neuron less responsive to released glutamate.
The complexity of serotonin's role in synaptic modulation is further demonstrated by its interaction with various other neurotransmitters and the impacts of diseases like Alzheimer's on serotonergic receptors density and functioning.