| Summary: | 碩士 === 慈濟大學 === 藥理暨毒理學研究所 === 94 === Neurons of the superficial spinal dorsal horn particularly those on substantia gelatinosa (SG) are known to play an important role in nociceptive transmission. We observed that intravenous injection of ethanol in rats dose-dependently increased the duration of tail-flick latency, suggesting that ethanol may play an inhibitory role in nociceptive processing. As far as we know, no documents examined the effect of ethanol on SG neurons. The present study examined the effects of ethanol on the activity of SG neurons of lumbar spinal cord slices from 13-21-day-old rats by whole cell patch recording. The results showed that ethanol (100 mM) applied by superfusion for 15 min had no significant effects on membrane potential and on the threshold and the amplitude of action potential of SG neurons. Superfusion of ethanol (50 and 100 mM) for 5 min dose-dependently decreased the amplitude of evoked excitatory postsynaptic potential (EPSP). Application of ethanol (100 mM) onto SG neurons significantly decreased glutamate-induced depolarizations. NMDA-induced depolarizations were significantly reduced following superfusion of ethanol for 15 minutes whereas ethanol had no significant effects on AMPA-induced responses. In order to determine the presynaptic effects of ethanol in SG neurons, we examined the actions of ethanol on miniature excitatory postsynaptic potential (mEPSPs). Application of ethanol (100 mM) for 5 minutes reversibly decreased mEPSC frequency and amplitude. Taking together, our data suggest that ethanol acts both pre-synaptically and post-synaptically on SG neurons to decrease the excitability of spinal dorsal horn neurons, leading to reductions in the nociceptive neurotransmission. These may account for a cellular basis for the anti-nociceptive action of ethanol at the spinal cord level.
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