Final answer:
The influx of calcium through postsynaptic NMDA receptors leads to short-term phosphorylation of AMPA receptors and long-term synaptic plasticity through LTP and LTD, key processes in synaptic strengthening and weakening respectively, which are crucial for learning and memory.
Step-by-step explanation:
The influx of calcium through postsynaptic NMDA receptors can trigger both short-term and long-term changes in the postsynaptic neuron. In the short-term, elevated calcium levels activate enzymes like CaMKII, leading to the phosphorylation and increased function of existing AMPA receptors which facilitate greater depolarization in response to glutamate, the primary excitatory neurotransmitter in the brain.
Long-term changes include synaptic plasticity in the forms of long-term potentiation (LTP) and long-term depression (LTD). LTP strengthens synaptic connections through the insertion of more AMPA receptors into the postsynaptic membrane, potentially resulting in a faster and more robust response to presynaptic glutamate release. Conversely, LTD weakens synaptic connections by removing AMPA receptors, making the postsynaptic neuron less responsive to glutamate. Both processes are essential for learning and memory, with LTP relating to the reinforcement of synaptic connections and LTD allowing for the pruning of less useful synaptic pathways.