Abstract
The orexin neuropeptide family consists of orexin-A and orexin-B, which are coded from the same prepro-mRNA. Although peripherally administered orexin-A abolishes small intestinal interdigestive contractions in rats, it still remains unclear whether orexin-A of lateral hypothalamic area(LHA) effects on the gastric motility in rats. We selected Wistar rats as our subjects. A stainless-steel injection cannula was implanted unilaterally into the LHA. A force transducer was embedmented into the stomach to record circular muscle contractiontions in freely moving conscious rats. The gastric motility was monitored by administration of ghrelin into LHA. The changes of amplitude of constriction and frequency of gastric motility were monitored in conscious rats by a transducer. Subdiaphragmatic vagotomy was performed to elucidate the neural pathways of orexin-A. After microinjection of orexin-A into LHA 5-20 min later, Orexin-A dose-dependently increased the amplitude of contraction and accelerated frequency of gastric motility in the stomach. The effect of orexin-A on promoting the amplitude and frequency of gastric contraction disappeared after 0.5μg orexin-A +6.0μg SB-334867 mixture was microinjection into LHA. However, there was no significant changes of amplitude and frequency of gastric contraction while injection of orexin-A receptor antagonists SB-334867 alone. The stimulatory effect of orexin-A on gastric motility was abolished by subdiaphragmatic vagotomy. It is suggested that exogenous orexin-A of LHA may promote gastric motility, the effect may be accomplished through the LHA-vagus pathway.
Highlights
The orexins consist of orexin-A and orexin-B, named hypocretin 1 and hypocretin 2.They are hypothalamic peptides produced in lateral hypothalamic neurons and released widely throughout the central nervous system(CNS) [1,2]
Administration of orexin-A into the dorsal motor nucleus of vagus (DMV) increased intragastric pressure and antral motility in anesthetized rats [11], the effects induced by orexin-A were attenuated by vagotomy[12].it is not clear whether hypothalamus administered orexin-A modulates the gastric motility in conscious rats
When 5.0 μg orexin-A was administrated into the LHA in subdiaphragmatic vagotomy rats, the amplitude and frequency of gastric contractions dramatically reduced compared with sham operation + orexin-A group, there was no significant change in subdiaphragmatic vagotomy group,subdiaphragmatic vagotomy + NS group and subdiaphragmatic vagotomy+orexin-A group (Fig. 2)
Summary
The orexins consist of orexin-A and orexin-B, named hypocretin 1 and hypocretin 2.They are hypothalamic peptides produced in lateral hypothalamic neurons and released widely throughout the central nervous system(CNS) [1,2]. Orexin-A and orexin-B regulate homeostatic mechanisms of energy balance and metabolism through activation of two G-protein coupled receptors[2,3], orexin receptors 1 and 2 (OX1R and OX2R, respectively). Recent studies have shown that orexin-A regulate gastrointestinal motility through the brain–gut axis[8]. The evidences suggest that central orexin-A plays a role in gastrointestinal motility through the vagal pathways[9]. Administration of orexin-A into the DMV increased intragastric pressure and antral motility in anesthetized rats [11], the effects induced by orexin-A were attenuated by vagotomy[12].it is not clear whether hypothalamus administered orexin-A modulates the gastric motility in conscious rats. The objective of our studies was to determine whether orexin-A administration into LHA affects gastric motility,and whether the effect of orexin-A is mediated by the vagal pathways
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