期刊:Oxford University Press eBooks [Oxford University Press] 日期:2004-12-09卷期号:: 61-97
标识
DOI:10.1093/acprof:oso/9780195178043.003.0003
摘要
This chapter reviews recent progress towards an understanding of synaptic plasticity resulting in increased synaptic efficacy as the main candidate for a cellular mechanism of memory. The most studied form of cellular plasticity is long-term potentiation (LTP). LTP is prominent in the hippocampus, develops rapidly, is long lasting, is specific to the synapses activated during experience, and can associate multiple stimuli. The LTP is based on concurrent input activation and depolarization, and involves a combination of AMPA and NMDA receptors for the neurotransmitter glutamate. Its maintenance depends on a cascade of molecular events. There is also a mechanism for long term depression (LTD) that involves reduction of synaptic efficacy and LTD is also dependent on AMPA and NMDA receptors. There is mounting evidence that LTP is indeed involved in memory, including changes in synaptic efficacy that occur following learning, and that preventing LTP blocks the formation of lasting memories.