Change in brain thyrotropin-releasing hormone (TRH) mechanism of amygdaloid kindled rats.
We reported previously that DN-1417, a potent analog of thyrotropin-releasing hormone (TRH), suppressed both the progression of amygdaloid (AM) kindling and AM kindled seizure. To study a functional role of the cerebral TRH mechanism in AM kindling, immunoreactive TRH (IR-TRH) and specific TRH receptor binding were examined in the rat brains kindled from the left AM. The IR-TRH concentration elevated significantly in the amygdala plus piriform cortex and the hippocampus 24 and 48 hours after the AM kindled convulsion. Such an elevation of IR-TRH was not found 7 days after the last convulsion, indicating that the elevation of IR-TRH was a transient change seen after the AM kindled convulsion. By contrast, the specific TRH receptor binding in the striatum increased 48 hours, 7 and 21 days after the AM kindled convulsion. This indicates that the increase of the specific TRH binding in the striatum was a long-lasting change. The present study suggests that the change in the striatal TRH receptors may be associated with a long-lasting seizure susceptibility of AM kindled rats.
D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001696:Biomechanical Phenomena; D001921:Brain / Q000378:metabolism*; D007696:Kindling, Neurologic; D008297:Male; D011863:Radioimmunoassay; D051381:Rats; D011919:Rats, Inbred Strains; D017981:Receptors, Neurotransmitter / Q000378:metabolism; D018025:Receptors, Thyrotropin-Releasing Hormone; D013973:Thyrotropin-Releasing Hormone / Q000378:metabolism*
D017981:Receptors, Neurotransmitter; D018025:Receptors, Thyrotropin-Releasing Hormone; D013973:Thyrotropin-Releasing Hormone