The spinal reflex of chronic spinal rats is supersensitive to 5-HTP but not to TRH or 5-HT agonists.

The effects of thyrotropin-releasing hormone (TRH), 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) and L-5-hydroxytryptophan (5-HTP) were studied on the monosynaptic reflex (MSR) and the polysynaptic reflex (PSR) in acute and chronic spinal rats. Radioimmunoassay showed that while chronic spinal transection (for 2 weeks) caused the complete depletion of TRH in the ventral lumbar enlargement a certain level of TRH was maintained in the dorsal lumbar enlargement. This result suggested the existence of TRH-containing neurons in the dorsal horn other than the medullary raphe neurons descending to the spinal cord. The latency to the start of the MSR was shortened in chronic spinal rats and the amplitudes of the MSR and PSR were significantly greater than those in acute spinal rats. There was no obvious difference in the effects of TRH and 5-MeODMT on spinal reflexes of acute and of chronic spinal rats although marked supersensitivity to 5-HTP was observed in both the MSR and the PSR in chronic spinal rats. The supersensitivity to 5-HTP was considered to be 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. It is suggested that TRH and 5-HT do not show any mutual requirement for each other in their effects on the spinal reflex since co-depletion of TRH and 5-HT did not change the effects of TRH and 5-MeODMT in chronic spinal rats. The coexistence of 5-HT and TRH in the descending spinal pathway is not considered to be significant for the control of spinal reflexes at the postsynaptic level.