Inhibition of long-term potentiation by NMDA-mediated nitric oxide release.
Activation of N-methyl-D-aspartate (NMDA) receptors before tetanic stimulation blocks long-term potentiation (LTP) in the CA1 region of the hippocampus. This NMDA-mediated inhibition of LTP can be reversed by the nitric oxide (NO) inhibitors L-NG-monomethyl-arginine or hemoglobin and mimicked by sodium nitroprusside. These results indicate that the timing of NO release relative to high-frequency activation of CA1 synapses may be an important determinant of LTP generation and suggest that NO may play a positive or negative modulatory role in LTP depending on prior events at the tetanized synapse and the ambient concentration of excitatory amino acids.
Izumi
Y
Y
Department of Psychiatry, Washington University School of Medicine, St. Louis, MO 63110.
Clifford
D B
DB
Zorumski
C F
CF
D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D004594:Electrophysiology; D006454:Hemoglobins / Q000494:pharmacology; D006624:Hippocampus / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D016202:N-Methylaspartate / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism*; D009599:Nitroprusside / Q000494:pharmacology; D051381:Rats; D013997:Time Factors; D019323:omega-N-Methylarginine
D006454:Hemoglobins; D009599:Nitroprusside; D019323:omega-N-Methylarginine; D009569:Nitric Oxide; D016202:N-Methylaspartate; D001120:Arginine