Response contingency and the dissipation of ethanol tolerance.
Ethanol (1.5 g/kg) administered intraperitoneally to kindled rats blocks the seizures normally elicited by electrical stimulation of the amygdala. Tolerance to this anticonvulsant effect develops following a series of ethanol injections delivered at 48-hr intervals only when an amygdaloid stimulation is administered during each period of ethanol intoxication. In the present study, the response contingency was shown to also play a critical role in the dissipation of tolerance. There was no significant loss of tolerance over a 14-day retention interval in rats that received: 1) bidaily ethanol injections each followed 1 hr later by a convulsive stimulation; or 2) bidaily ethanol injections but no stimulation; or 3) neither ethanol nor stimulation. In contrast, tolerance dissipated completely in rats that received: 1) bidaily stimulations but no ethanol; or 2) convulsive stimulation 1 hr before each bidaily ethanol injection. Accordingly, the cessation of ethanol exposure was neither necessary nor sufficient for the dissipation of tolerance to the anticonvulsant effect of ethanol. The critical factor in the decline of tolerance was the elicitation of seizures in the absence of ethanol.
Department of Psychology, University of British Columbia, Vancouver, Canada.
M J
MJ
Mana
J P
JP
Pinel
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology; D004361:Drug Tolerance; D000431:Ethanol / Q000494:pharmacology*; D007696:Kindling, Neurologic / Q000187:drug effects; D008297:Male; D051381:Rats; D012640:Seizures / Q000503:physiopathology*
D000927:Anticonvulsants; D000431:Ethanol