TY - JOUR
T1 - Modulation of LTP induction by NMDA receptor activation and nitric oxide release
AU - Zorumski, C. F.
AU - Izumi, Y.
N1 - Funding Information:
The work in the authors’ lab was supported by NIMH Research Scientist Development Award MH00964, grants MH45493 and AG11355, and the Bantly Foundation.
PY - 1998
Y1 - 1998
N2 - In the CA1 hippocampal region, the induction of long-term potentiation (LTP) requires activation of N-methyl-D-aspartate receptors (NMDARs). However, untimely NMDAR activation either immediately prior to or following tetanic stimulation inhibits LTP generation. This NMDAR-mediated LTP inhibition is overcome by inhibitors of nitric oxide synthase (NOS) and hemoglobin, suggesting the involvement of NO. Additionally, NO inhibitors can promote the ability of weak tetanic stimuli to produce LTP under basal conditions in hippocampal slices. Recent experiments indicate that untimely NMDAR activation contributes to the failure of LTP induction during periods of low glucose exposure and hypoxia. Following hypoxia there is also a delayed form of LTP inhibition that is reversed by NMDAR antagonists and NO inhibitors. These results suggest that there are physiological and pathological conditions during which NMDAR activation and NO release modulate the induction of synaptic plasticity.
AB - In the CA1 hippocampal region, the induction of long-term potentiation (LTP) requires activation of N-methyl-D-aspartate receptors (NMDARs). However, untimely NMDAR activation either immediately prior to or following tetanic stimulation inhibits LTP generation. This NMDAR-mediated LTP inhibition is overcome by inhibitors of nitric oxide synthase (NOS) and hemoglobin, suggesting the involvement of NO. Additionally, NO inhibitors can promote the ability of weak tetanic stimuli to produce LTP under basal conditions in hippocampal slices. Recent experiments indicate that untimely NMDAR activation contributes to the failure of LTP induction during periods of low glucose exposure and hypoxia. Following hypoxia there is also a delayed form of LTP inhibition that is reversed by NMDAR antagonists and NO inhibitors. These results suggest that there are physiological and pathological conditions during which NMDAR activation and NO release modulate the induction of synaptic plasticity.
UR - http://www.scopus.com/inward/record.url?scp=0031740696&partnerID=8YFLogxK
U2 - 10.1016/s0079-6123(08)63207-0
DO - 10.1016/s0079-6123(08)63207-0
M3 - Review article
C2 - 9932441
AN - SCOPUS:0031740696
VL - 118
SP - 173
EP - 182
JO - Progress in Brain Research
JF - Progress in Brain Research
SN - 0079-6123
ER -