Long‐Term Increase in Striatal Thyrotropin‐Releasing Hormone Receptor Binding Caused by Amygdaloid Kindling

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Abstract
Summary: : Our previous finding that intracerebroven‐tricular (i.e.v.) administration of both thyrotropin‐releasing hormone (TRH) and its analogue, γ‐butyro‐lactone‐γ‐carbonyl‐L‐histidyl‐L‐prolinamide citrate (DN‐1417), suppressed seizure development of amygdaloid (AM) kindling and kindled AM seizures leads to a new hypothesis that endogenous TRH may be an antiepi‐leptic substance in the brain. In this study, we examined postictal chronological changes in both immunoreactive TRH (IR‐TRH) and TRH receptor binding activity in discrete brain regions of AM‐kindled rats to study the relationship of the brain TRH system to kindling‐induced seizure susceptibility. AM‐kindled rats were decapitated 30 min, 24 h, 48 h, 7 days, and 21 days after the last kindled convulsion. IR‐TRH increased markedly in the AM/pyri‐form cortex and hippocampus 24 and 48 h after the last convulsion, and returned to the control (unstimulated, sham‐operated) value within 3 weeks after the convulsions ended. In contrast, a significant increase in the striatal TRH binding sites was evident 24 h after the cessation of convulsions which lasted 21 days. A lasting change in the striatal TRH neural system may be related to kindling‐induced seizure susceptibility.