Abstract

Injection of 30 mg/kg of pilocarpine 24 h after systemic injection of lithium (3 mEq/kg) results in overt limbic motor seizures within about 30 min. Results of several experiments indicated that whereas food deprivation or repeated nociceptive stimulation during the previous 24 h decreased seizure onset times (SOTs) by about 11 to 12 min, food restriction, continuous lighting, or, handling during the previous 7 to 14 days increased SOTs by comparable durations. Early handling before weaning but not injections of clomimpramine also decreased SOTs. A difference of 18 min in the means of SOTs was produced by injecting either 1.0 (increased SOT) or 1.5 mg/kg (decreased SOT) of dexamethasome during the previous 24 h. A strong (multiple r=.87) association between SOTs and the amount of damage within five specific thalamic–limbic nuclei was observed. These results, in conjunction with blood corticosterone levels taken before and after induction of the seizures, suggest the neurochemical mechanisms affecting the range in SOTs could involve the adrenocorticotropic hormone (ACTH)–corticosterone system and influence the amount of post-seizure-induced damage.

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