The intersections of NMDAR-dependent synaptic plasticity and cell survival.
The discovery of a requirement for N-methyl d-aspartate receptor (NMDAR) activation in long-term potentiation (LTP) set off an explosion of interest in the mechanisms of NMDAR-dependent synaptic plasticity. Meanwhile other research has advanced our understanding of how NMDAR activation regulates neuronal death and survival. Surprisingly, there have been few attempts to correlate these important areas of research. Here we review current knowledge of the various mechanisms of NMDAR-dependent synaptic plasticity that are shared with neuronal survival and death, while drawing comparisons with the proneurotrophin/neurotrophin receptor and intracellular signaling systems. Our conclusion is that NMDAR-dependent LTP and long-term depression (LTD) share many common mechanisms with cell survival and cell death, respectively. The intersections of plasticity and cell survival may represent novel avenues for neuroprotection. This article is part of the Special Issue entitled 'Glutamate Receptor-Dependent Synaptic Plasticity'.
Brain Research Centre, Room F270, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC V6T 2B5, Canada.
Thomas E
TE
Bartlett
Yu Tian
YT
Wang
D000818:Animals; D002470:Cell Survival / Q000502:physiology; D008959:Models, Neurological; D009410:Nerve Degeneration / Q000503:physiopathology*; D009473:Neuronal Plasticity / Q000502:physiology*; D016194:Receptors, N-Methyl-D-Aspartate / Q000502:physiology*; D017475:Receptors, Nerve Growth Factor / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology
D016194:Receptors, N-Methyl-D-Aspartate; D017475:Receptors, Nerve Growth Factor
AMPA receptor; BDNF; Cell survival; LTD; LTP; NMDA receptor; Neurotrophin; Synaptic plasticity