Thyrotropin-releasing hormone (TRH) and CNS regulation of anorectal motility in the rat

Abstract

The effect of thyrotropin-releasing hormone (TRH) upon anorectal motility was investigated in acute male rat preparations. Micromolar doses of TRH were intrathecally (i.t.) infused at the L6 spinal level at a rate of 1 μl/min over 8 min. TRH infusions in 1.0–1000 μM concentrations elicited biphasic, dose-dependent anorectal contractions as measured by a rectal manometer. The 100 μM dose yielded the most significant increase in contractions over the greatest period of time. Atropine, administered as a pretreatment (100 μg s.c.), blocked contractions normally produced by i.t. infusion of TRH (1000 μM). Intravenous infusions of atropine (10 μg) through a jugular catheter immediately blocked anorectal contractions produced by i.t. infusion of 100 μM TRH. Sectioning of the hypogastric nerve, which supplies sympathetic innervation to the colon and internal anal sphincter, did not significantly affect contractions induced by 100 μM TRH applied intrathecally. Disruption of the major pelvic ganglion fibers, however, completely abolished the contractions induced by 100 μM TRH, either through the interruption of preganglionic parasympathetic fibers in the pelvic nerve, or by disrupting postganglionic fibers. These findings extend the role of TRH in the regulation of defecatory behaviors.