THYROTROPIN-RELEASING-HORMONE (TRH) HAS INDEPENDENT EXCITATORY AND MODULATORY ACTIONS ON LAMINA-IX NEURONS OF LUMBOSACRAL SPINAL-CORD SLICES FROM ADULT-RATS

Coronal and horizontal slices of the lumbar and sacral spinal cord, re spectively, of ovariectomized adult rats, either treated with estrogen (OVX + E) or untreated (OVX), were used to test the neuronal actions of TRH and its metabolite, cyclo(His-Pro) (or cHP). Both coronal slice s, which possess only short stumps of ventral roots (VRs), and horizon tal slices, in which long sections of VRs were preserved, were used fo r extracellular recording of single motor and other types of neurons. Methodological comparisons between these two types of slices showed th at the length of VRs preserved had no significant effect on the charac teristics of motoneurons (MNs). In coronal slices, MNs in medial and l ateral lamina IX (MN(M) and MN(L), respectively) were identified by an tidromic activation. Of these lumbar MNs, estrogen treatment lowered t he antidromic activation threshold for MN(M) but not MN(L). Because MN (M) innervate the back muscles crucial for the execution of the estrog en-dependent lordosis, the observed estrogen effect may contribute to the hormone's induction of the sexual behavior. The recorded MNs and o ther types of neurons were subjected to bath applications of TRH, cHP, and neurotransmitters. TRH was found to be capable of evoking an earl y, shorter-lasting neuronal excitation and/or a late, longer-lasting m odulation of neuronal responses to transmitters. Each neuronal action could occur with or without the other, and the occurrence of the excit ation did not affect the probability of whether a modulation would occ ur later. The modulatory, but not the excitatory, action appeared to b e shared by cHP, because cHP could also modulate neuronal responses in similar, if not identical, ways as TRH did, but could neither stimula te neurons nor mimic TRH in desensitizing TRH-evoked excitation. The m odulatory actions of the two peptides were not affected by estrogen. A lthough the excitatory action was desensitized by repeated TRH applica tions, the modulatory action did not appear to be attenuated but inste ad was often enhanced by repeated administrations of TRH and/or cHP. T hese results, together with the essentially identical findings from ou r previous study on hypothalamic neurons, indicate that the excitatory and the modulatory actions of TRH are independent of each other and, hence, are mediated by different subcellular mechanisms.