The Study of TRH-containing Nervous Systems in the Spinal Cord

Research Project

Project/Area Number	60571035
Research Category	Grant-in-Aid for General Scientific Research (C)
Allocation Type	Single-year Grants
Research Field	Biological pharmacy
Research Institution	The University of Tokyo
Principal Investigator	ONO Hideki Faculty of Pharmaceutical Sciences, The University of Tokyo, 薬学部, 助教授 (00080200)
Project Period (FY)	1985 – 1986
Project Status	Completed (Fiscal Year 1986)
Budget Amount *help	¥400,000 (Direct Cost: ¥400,000) Fiscal Year 1986: ¥400,000 (Direct Cost: ¥400,000)
Keywords	TRH / Serotonin / Spinal cord / スーパーセンシィティビティ
Research Abstract	Destruction of descending serotonergic nerve terminals containing thyrotropin-releasing hormone (TRH) was effected in rats by the intracisternal injection of 5,6-dihydroxytryptamine (5,6-DHT) two weeks before subsequent examinations. Although the level of TRH in the lumbar enlargement was significantly reduced in 5,6-DHT-treated rats, the effects of TRH on the monosynaptic reflex (MSR) and polysynaptic reflex (PSR) in these rats were not different from those in control rats. MSR inhibition by 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) was attenuated by 5,6-DHT treatment, although there was no obvious difference in the effects of 5-MeODMT on the PSR between 5,6-DHT-treated and control rats. In 5,6-DHT-treated rats, L-5-hydroxytryptophan (5-HTP) markedly decreased the MSR and increased the PSR, although the same doses of 5-HTP did not produced any effects on either the MSR or PSR in control rats. In control rats, after administration of imipramine or clorgyline, 5-HTP produced effects similar to those observed in 5,6-DHT-treated rats. These results suggest that the supersensitivity to 5-HTP in 5,6-DHT-treated rats is due to a lack of 5-hydroxytryptamine (5-HT) uptake into 5-HT-containing nerve terminals rather than to a change in 5-HT receptors.