Abstract
TRH is found in terminals in the dorsal, lateral, and ventral horns of the spinal cord and apparently has at least a weak facilitatory effect on excitability of neurons in all these locations. These findings suggest that TRH may facilitate transmission in somatosensory pathways, enhance sympathetic outflow from the spinal cord, and facilitate somatic motoneuron excitability, at least transiently. All studies that have examined TRH effects on spinal neuronal excitability have used exogenously administered TRH. Virtually nothing is known about how spinal neuronal functioning might be affected by TRH released from terminals after activation of TRH-containing cell bodies. The acquisition of this knowledge awaits the development of specific TRH antagonists. Preliminary experiments suggest that TRH may have prolonged facilitatory effects on the excitability of developing or damaged spinal cord neurons. Further studies are necessary to determine how TRH interacts with other neuroactive peptides and monoamines to affect excitability of neurons in the developing, damaged, and normal adult spinal cord.
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