NMDA receptor-independent LTP in mammalian nervous system

Long-term potentiation (LTP) of synaptic transmission is a form of activity-dependent synaptic plasticity that exists at most synapses in the nervous system. In the central nervous system (CNS), LTP has been recorded at numerous synapses and is a prime candidate mechanism associating activity-dependent plasticity with learning and memory. LTP involves long-lasting increase in synaptic strength with various underlying mechanisms. In the CNS, the predominant type of LTP is believed to be dependent on activation of the ionotropic glutamate Nmethyl-D-aspartate receptor (NMDAR), which is highly calcium-permeable. However, various forms of NMDARindependent LTP have been identified in diverse areas of the nervous system. The NMDAR-independent LTP may require activation of glutamate metabotropic receptors (mGluR) or ionotropic receptors other than NMDAR such as nicotinic acetylcholine receptor (alpha 7-nAChR), serotonin 5-HT3 receptor or calcium-permeable AMPA receptor (CP-AMPAR). In this review, NMDAR-independent LTP of various areas of the central and peripheral nervous systems are discussed.

Automated summary

Long-term potentiation (LTP) is a form of activity-dependent synaptic plasticity that is closely associated with learning and memory. In the central nervous system, the activation of NMDAR is believed to be the main mechanism causing LTP, although other NMDAR-independent forms of LTP also exist.