Seizures and thyrotropin-releasing hormone (TRH) neural system in the rat brain.
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.
D000818:Animals; D001921:Brain / Q000378:metabolism*; D008297:Male; D010433:Pentylenetetrazole; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000139:chemically induced / Q000378:metabolism* / Q000517:prevention & control; D013973:Thyrotropin-Releasing Hormone / Q000031:analogs & derivatives / Q000378:metabolism* / Q000627:therapeutic use; D014018:Tissue Distribution
D013973:Thyrotropin-Releasing Hormone; C029762:DN 1417; D010433:Pentylenetetrazole