Ventral root depolarization and spinal reflex augmentation by a TRH analog in rat spinal cord.

The experiments were performed on spinal rats transected at the C 1 level. Intravenous administrations of TRH and its analog DN-1417 (gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide), which has less endocrine activity, produced a marked increase in the monosynaptic reflex (MSR) and depolarization of the ventral root, without affecting the dorsal root reflex (DRR) and the resting potential of the dorsal root. Excitation of the monosynaptic reflex was not antagonized by chlorpromazine, haloperidol, atropine or cyproheptadine, and was not influenced by pretreatment with reserpine. The depolarization of the ventral root persisted in the presence of baclofen or tetrodotoxin. These findings suggest that depolarization of the ventral root induced by TRH and DN-1417 is due to a direct action on motoneuronal membranes, and that an increase in the monosynaptic reflex is in part due to a depolarization of motoneurones. The effect of DN-1417 were longer lasting than those of TRH.