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, 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.

• Authors: S Kajita, M Nakashima, M Okamoto, M Sato, N Ogawa
• Journal: The Japanese journal of psychiatry and neurology (Jpn J Psychiatry Neurol) Vol. 40 Issue 3 Pg. 345-7 (Sep 1986) ISSN: 0912-2036 [Print] Japan
• PMID: 3033370 (Publication Type: Journal Article)

Chemical References

• Receptors, Neurotransmitter
• Receptors, Thyrotropin-Releasing Hormone
• Thyrotropin-Releasing Hormone

Topics

• Amygdala (physiology)
• Animals
• Biomechanical Phenomena
• Brain (metabolism)
• Kindling, Neurologic
• Male
• Radioimmunoassay
• Rats
• Rats, Inbred Strains
• Receptors, Neurotransmitter (metabolism)
• Receptors, Thyrotropin-Releasing Hormone
• Thyrotropin-Releasing Hormone (metabolism)