Change in Brain Thyrotropin‐Releasing Hormone (TRH) Mechanism of Amygdaloid Kindled Rats

Abstract

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, immuno‐reactive 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.