Role of nitric oxide in NMDA-evoked release of [3H]-dopamine from striatal slices.
Evidence that excitatory amino acids act via N-methyl-D-aspartate (NMDA) receptors to evoke the release of catecholamines from axonal terminals and synaptosomes has been used to argue for the presence of pre-synaptic NMDA receptors. NMDA receptor agonists also generate nitric oxide (NO) which rapidly diffuses through neural tissue. We find that exogenously applied NO evokes [3H]-dopamine release from cultured neurons. This release is not blocked by the NMDA antagonist MK-801 nor by tetrodotoxin. Both NG-nitroarginine which inhibits NO synthesis, and hemoglobin which binds extracellular NO, block NMDA-evoked [3H]-dopamine release from striatal slices. A major role of endogenously-synthesized NO may be to evoke neurotransmitter release in local volumes of neural tissue.
Hanbauer
I
I
Laboratory of Chemical Pharmacology, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.
Wink
D
D
Osawa
Y
Y
Edelman
G M
GM
Gally
J A
JA
D000818:Animals; D002478:Cells, Cultured; D003342:Corpus Striatum / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism*; D005260:Female; D066298:In Vitro Techniques; D016202:N-Methylaspartate / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D014316:Tritium
D014316:Tritium; D009569:Nitric Oxide; D016202:N-Methylaspartate; D004298:Dopamine