Premium
Sensitivity to Strychnine Seizures Is Unaltered during Ethanol Withdrawal
Author(s) -
Gonzalez Larry P.
Publication year - 1993
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1993.tb05659.x
Subject(s) - strychnine , picrotoxin , inhibitory postsynaptic potential , ethanol , convulsion , glycine receptor , anesthesia , central nervous system , antagonist , epilepsy , psychology , neuroscience , chemistry , medicine , glycine , receptor , biochemistry , amino acid
Previous research from this laboratory has indicated that animals chronically exposed to ethanol and then withdrawn exhibit a variety of symptoms of central nervous system hyperexcitability that occur in unique clusters.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 withdrawal. In addition, the observed clusters of spontaneous seizure events in these animals were seen to correlate with differences in sensitivity to seizure‐inducing treatments. These results suggest that seizure sensitivity during ethanol withdrawal may indicate the involvement of multiple, independent, neuronal mechanisms. To investigate this possibility further, the following study examined the sensitivity of ethanol‐withdrawn animals to seizures induced by the glycine antagonist strychnine. Seizure sensitivity to strychnine was evaluated at the same times following ethanol withdrawal when animals were previously seen to show the differential occurrence of spontaneous seizure events and also differences in sensitivity to picrotoxin‐induced seizures. Ethanol‐withdrawn animals did not differ in their responses to strychnine compared with ethanol‐naive controls at any of the times tested. This lack of change in seizures induced by antagonism of glycine inhibition occurred in spite of the increased sensitivity of similarly treated animals to picrotoxin‐induced seizures at the same test times. These data suggest that chronic ethanol exposure and withdrawal may not significantly alter the function of glycinergic inhibitory neurotransmission and that the ethanol withdrawal syndrome is indicative of alterations in specific neuronal mechanisms rather than of a generalized state of central nervous system hyperexcitability.