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Seizures and Thyrotropin‐Releasing Hormone (TRH) Neural System in the Rat Brain
Author(s) -
Ogawa Norio,
Kajita Saburo,
Sato Mitsumoto,
Mori Akitane
Publication year - 1985
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1111/j.1440-1819.1985.tb02007.x
Subject(s) - thyrotropin releasing hormone , kindling , medicine , endocrinology , hippocampus , pentylenetetrazol , chemistry , thalamus , epilepsy , hormone , neuroscience , psychology , anticonvulsant
. In order to study the relationship between seizures and the thyrotropin‐releasing hormone (TRH) neural system, immunoreactive TRH (IR‐TRH) and TRH receptor binding activity were determined by pentylenetetrazol (PTZ)‐induced seizures and amygdaloid (AM) kindling. IR‐TRH markedly increased in the septum 40 and 150 seconds after the PTZ injection. A significant increase in the IR‐TRH concentrations was also noted in the hippocampus and thalamus/midbrain 40 and 150 seconds after the PTZ injection, respectively. However, no significant changes were observed in the TRH receptor binding before, during or after the PTZ‐induced seizures. In addition, a lasting change in the striatal TRH receptors after AM kindling as well as a transient IR‐TRH increase in the limbic structures were seen 48 hours after AM‐kindled convulsions. TRH and its analog (DN‐1417) inhibited PTZ‐induced generalized seizures dose‐dependently. These findings indicate the involvement of the TRH neural system in seizure mechanisms, and suggest that endogenous TRH may be an antiepileptic substance in the brain.