Abstract
The central, but not the peripheral, administration of TRH elicited an increase in the gastrointestinal (GI) motor activity in anesthetized rabbits. This effect did not appear to be mediated via the pituitary-thyroid axis and it was relatively independent of the degree of basal motor activity in the GI tract. I.v. administration of either atropine or ganglionic blocking agents antagonized this phenomenon. Bilateral vagal transection prevented the TRH-induced stimulation of GI motor activity, but neither spinal transection nor i.v. guanethidine had any effect. When injected into the lateral ventricles, 3rd ventricle or cisterna magna, TRH always elicited its GI effects. Central cholinergic mechanisms appear to be involved because both atropine methyl bromide and atropine sulfate given i.c.v. antagonized the GI effects. I.v. injection of phenoxybenzamine also inhibited the TRH effect. TRH stimulates neural pathways within the CNS to activate efferent vagal fibers leading to a generalized increase in the motor activity of the GI tract.

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