The role of monoaminergic systems in central IL‐1β‐induced changes in intestinal motility

Abstract

Abstract Intracerebroventricular (i.c.v.) injection of interleukin‐1β (IL‐1β) in fed rats induces stimulation of caecocolonic contractions, involving corticotropin‐releasing factor (CRF) and the reappearance of the fasted motor pattern (presence of migrating myoelectric complexes, MMCs) at the small intestinal level, which is mediated by prostaglandins (PGs). The mechanisms of these effects were further investigated by focusing on the possible involvement of central monoaminergic systems. Motility was appraised in conscious rats chronically implanted with electrodes in the jejunum and caecum, and a catheter in a lateral ventricle of the brain. IL‐1β (15 ng, i.c.v.) was administered in fed rats that were untreated, or after previous administration of either antagonists of α1 and α2 adrenergic (prazocin and yohimbine), D1 and D2 dopaminergic (SCH 23390 and sulpiride) and 5HT3 serotonergic (granisetron) receptors. Only prazocin and yohimbine (1 mg kg−1 i.p.) significantly reduced the duration of the MMC pattern induced by IL‐1β at the jejunal level (78 ± 35 min and 40 ± 12 min, respectively, vs 223 ± 48 min in control studies). In contrast, the caecal stimulation triggered by IL‐1β was not only blocked by prazocin and yohimbine (1 mg kg−1 i.p.), but also by sulpiride (1 mg kg−1 i.p.) and granisetron (1 mg kg−1 i.p.). This study confirms that IL‐1‐induced changes in small and large intestinal motility are expressed through two separate pathways. We can suggest that mediators acting to modulate CRF release, such as catecholamines through α1 and α2 receptors, dopamine through D2 receptors, and serotonin through 5HT3 receptors, could be involved in the caecal stimulation. PG‐dependent changes in the jejunal motility pattern seem to be linked to activation of α adrenoceptors.