Synaptic connections may be modified by many different forms of plasticity or adaptive processes. At some hippocampal synapses, such as the perforant path to granule cell synapse, long-term potentiation (LTP) is observed to decay over a period of days or weeks. LTP has attracted a great deal of interest as a possible synaptic mechanism of both learning and memory. NMDA, AMPA and metabotropic gluta-mate receptors are involved in the induction of LTP. Inhibitors of protein kinase C and CaMK II can decrease the induction of LTP. In addition, the phenomenon of long-term depression (LTD) is generally defined as a lasting , non pathological decrease in the strength of synaptic transmission. Several forms of hippocampal synaptic plasticity are dependent on calcium, providing a potential link between altered calcium homeostasis and memory deficits. Finally, psychosocial factors can have significant positive and negative effects on hippocampal structure and function.
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