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Vol. 280, Issue 3, 1341-1348, 1997
Department of Medicinal Chemistry and Molecular Pharmacology (P.S.,
P.G.G., J.L.B., G.E.I.) and
Department of Biological Sciences (S.G.R.),
Purdue University, West Lafayette, Indiana
The effect of cyanide on the N-methyl-D-aspartate (NMDA)-stimulated
increase in cytosolic free calcium ([Ca++]i)
was studied by microfluorescence in fura-2-loaded cerebellar granule
cells. The response to NMDA was enhanced by NaCN over a concentration
range of 20 to 100 µM. These concentrations of NaCN in the absence of
NMDA had no effect on basal [Ca++]i. In
comparison, NaCN did not affect K+-depolarization-induced
[Ca++]i elevation. The NaCN potentiation of
NMDA-evoked [Ca++]i elevation was blocked by
addition of Mg++ and by the NMDA receptor antagonists
2-amino-5-phosphono-valeric acid and
(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohept-5,10-imine maleate. Pretreatment of the cells with pregnenolone sulfate or arachidonate, known modulators of the NMDA receptor, enhanced NaCN
action. The voltage-sensitive calcium channel blockers nifedepine and
diltiazem did not affect the NaCN-induced potentiation. Additionally, the NaCN action was not altered when tetrodotoxin was used to block
Na+ channel-mediated glutamate release. In patch-clamp
studies, NaCN increased the amplitude and duration of NMDA-stimulated
whole-cell currents. NaCN also enhanced the NMDA receptor response in
single-channel patch-clamp experiments. In the outside-out patch
recording configuration, NaCN increased the NMDA receptor channel
opening frequency without affecting single-channel conductance or mean
channel open time. These results indicate that cyanide interacts
directly with the NMDA receptor channel complex to enhance
receptor-mediated responses.
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