Abstract |
Our previous finding that intracerebroventricular (i.c.v.) administration of both thyrotropin-releasing hormone (TRH) and its analogue, gamma-butyrolactone-gamma-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 antiepileptic 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/pyriform 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.
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Authors | S Kajita, N Ogawa, M Sato |
Journal | Epilepsia
(Epilepsia)
1987 May-Jun
Vol. 28
Issue 3
Pg. 228-33
ISSN: 0013-9580 [Print] United States |
PMID | 3034560
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Receptors, Neurotransmitter
- Receptors, Thyrotropin-Releasing Hormone
- Thyrotropin-Releasing Hormone
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Topics |
- Amygdala
(physiology)
- Animals
- Brain
(metabolism)
- Kindling, Neurologic
- Male
- Radioimmunoassay
- Radioligand Assay
- Rats
- Rats, Inbred Strains
- Receptors, Neurotransmitter
(metabolism)
- Receptors, Thyrotropin-Releasing Hormone
- Thyrotropin-Releasing Hormone
(metabolism)
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