Lp. Gonzalez, SENSITIVITY TO STRYCHNINE SEIZURES IS UNALTERED DURING ETHANOL WITHDRAWAL, Alcoholism, clinical and experimental research, 17(5), 1993, pp. 1029-1034
Previous research from this laboratory has indicated that animals chro
nically exposed to ethanol and then withdrawn exhibit a variety of sym
ptoms of central nervous system hyperexcitability that occur in unique
clusters. These clusters of symptoms were observed to differ in their
duration and in the time of onset relative to the time of ethanol wit
hdrawal. In addition, the observed clusters of spontaneous seizure eve
nts in these animals were seen to correlate with differences in sensit
ivity to seizure-inducing treatments. These results suggest that seizu
re sensitivity during ethanol withdrawal may indicate the involvement
of multiple, independent, neuronal mechanisms. To investigate this pos
sibility further, the following study examined the sensitivity of etha
nol-withdrawn animals to seizures induced by the glycine antagonist st
rychnine. Seizure sensitivity to strychnine was evaluated at the same
times following ethanol withdrawal when animals were previously seen t
o show the differential occurrence of spontaneous seizure events and a
lso differences in sensitivity to picrotoxin-induced seizures. Ethanol
-withdrawn animals did not differ in their responses to strychnine com
pared with ethanol-naive controls at any of the times tested. This lac
k of change in seizures induced by antagonism of glycine inhibition oc
curred in spite of the increased sensitivity of similarly treated anim
als to picrotoxin-induced seizures at the same test times. These data
suggest that chronic ethanol exposure and withdrawal may not significa
ntly alter the function of glycinergic inhibitory neurotransmission an
d that the ethanol withdrawal syndrome is indicative of alterations in
specific neuronal mechanisms rather than of a generalized state of ce
ntral nervous system hyperexcitability.