| Summary: | 碩士 === 國立臺灣大學 === 藥理學研究所 === 83 === We attempted in this study to explore the action of low concen-tration of cyanide on the synaptic transmission in the CA1 re-gion of rat hippocampal slices. Bath application of cyanide (30μM) could result in a transient and reversible depression on population spike (PS) and excitatory postsynaptic potential (EPSP). Sequential addition of cyanide (10-100μM) resulted in dose-dependent reduction of evoked PS and EPSP.Neither of the other oxidative phosphorylation uncouplers, sodium azide and 2,4-dinitrophenol, nor Na+ pump inhibitor, ouabain could mimick micromolar cyanide to induce a transient and reversible depression of CA1 evoked PS. Cyanide-induced transient depression of CA1 evoked PS was attenuated by L-type Ca2+channel blockers nifedipine, verapamil and NMDA receptor
antagonist 2-amino-5-phosphonopentanoic acid (APV),respectively,
indicating a possibility that the action of cyanide was partly
mediated by a postsynaptic NMDA receptor or a release of
transmitter which could be in a Ca2+-dependent release manner.
In the presence of adenosine A1 receptor antagonist 1,3-dipropyl 8-cyclopentylxanthine (DPCPX), the cyanide-induced inhibition was markedly reduced. Adenosine and adenosine uptake inhibitor dipyridamole could potentiate the cyanide-induced inhibition.
The cyanide-induced inhibition could be antagonized by diazoxide and potentiated by glibenclamide. The cyanide-induced depression of CA1 evoked PS was accompanied by an increase in the pair-pulse facilitation (PPF) ratio. Thus, the presynaptic
transmitter release is decreased during cyanide application.
When cyanide was applied immediately after high frequency
stimulation, not only post-tetanic potentiation was inhibited
but also long-term potentiation was blocked. However, when the
adenosine A1 receptor antagonist DPCPX was present, the
inhibitory effect of cyanide on evoked responses was markedly
reduced.
|
|---|
