Metabolic and behavioral consequences of lidocaine-kindled seizures.
Daily administration of lidocaine results in progressive increases in frequency and duration of convulsions in response to a dose of drug which was previously subconvulsive--a pharmacological kindling phenomenon. The effects of such lidocaine-kindling on local cerebral glucose utilization were determined by the 2-[14C]deoxyglucose method. Lidocaine-treated animals, in the absence of convulsions, exhibited decreased glucose utilization in most brain structures compared to saline-treated animals and showed no increase in aggressive behavior. In animals displaying lidocaine-kindled convulsions there were marked increases in glucose utilization in either the hippocampus and amygdala or in perirhinal cortical areas during the seizure administration; these animals also displayed long-lasting increases in irritable behavior. Seizure duration was positively correlated with the rate of glucose utilization in the hippocampus, amygdala and septum, but inversely correlated in several non-limbic areas. These data suggest that lidocaine-kindled seizures are highly localized to limbic and perirhinal structures and are associated with important behavioral consequences.
D000374:Aggression / Q000187:drug effects; D000679:Amygdala / Q000378:metabolism; D000818:Animals; D004597:Electroshock; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008012:Lidocaine / Q000494:pharmacology*; D008032:Limbic System / Q000378:metabolism*; D008297:Male; D010433:Pentylenetetrazole / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000139:chemically induced* / Q000378:metabolism / Q000523:psychology
D008012:Lidocaine; D005947:Glucose; D010433:Pentylenetetrazole