Analysis of the Control of Intestinal Motility in Fasted Rats, with Special Reference to Neurotensin

Abstract

Migrating myoelectric complexes (MMC) in the small intestine of fasted rats were monitored by means of four bipolar electrodes chronically implated at 5, 15, 25, and 35 cm distal to the pylorus. In intact rats the MMC occurred at regular intervals. Truncal abdominal vagotomy did not influence the initiation and propagation of the MMC. Administration of atropine, hexamethonium, or somatostatin significantly decreased the spiking activity of the MMC by 30–45% in the duodenum and jejunum. Infusion of neurotensin at two different doses (3.6 or 7 pmol × kg^-1 × min^-1) interrupted the activity front of the MMC and induced irregular spiking activity at all recording levels in control rats. In vagotomized rats neurotensin interrupted the activity front inconsistently. After atropine or hexamethonium administration, infusion of neurotensin did not interrupt the distal propagation of the activity front in the jejunum. Guanethidine, naloxone, Cimetidine, mepyramine. haloperidol. and a substance P antagonist did not change the MMC or alter the normal response to neurotensin. The results suggest that the inhibitory effect of neurotensin on the propagation of the jejunal activity front involves activation of enteric cholinergic mechanisms. Neurotensin seems to induce irregular spiking activity by a direct myogenic action. The enteric cholinergic innervation of the small intestine partially contributes to the occurrence of the spiking activity of the MMC in fasted rats.

Key words:

• Enteric nervous system
• migrating myoelectric complex
• neurotensin
• vagotomy