Abstract
Orexin-A is a circulating neuropeptide and neurotransmitter that regulates food intake and gastric motility. The central nucleus of the amygdala (CeA), which regulates feeding behavior and gastric function, expresses the orexin-1 receptor. The aim of this study was to evaluate the effects of microinjection of exogenous orexin-A into the CeA, on food intake and gastric motility, and to explore the mechanisms of these effects. Normal chow and high fat food (HFF) intake were measured, gastric motility and gastric emptying were evaluated, extracellular single unit firing was recorded, and c-fos expression was determined. The results showed that microinjection of orexin-A into the CeA resulted in increased HFF intake but did not affect normal chow intake. This effect was blocked by an orexin-1 receptor antagonist-SB-334867 and was partially blocked by a dopamine D1 receptor antagonist-SCH-23390. Gastric motility and gastric emptying were enhanced by orexin-A, and the former effect was abolished by subdiaphragmatic vagotomy. The firing frequency of gastric distention-related neurons was regulated by orexin-A via the orexin-1 receptor. Furthermore, c-fos expression was increased in the ventral tegmental area (VTA) and the nucleus accumbens (NAc), the lateral hypothalamus (LHA), and the dorsal motor nucleus of the vagus (DMV) in response to microinjection of orexin-A into the CeA. These findings showed that orexin-A regulated palatable food intake and gastric motility via the CeA. The LHA, the VTA, and the NAc may participate in palatable food intake and the CeA-DMV-vagus-stomach pathway may be involved in regulating gastric motility through the regulation of neuronal activity in the CeA.
Highlights
Food intake is regulated by several interrelated brain regions, including the hypothalamus, the hindbrain, and the limbic system (Merali et al, 2013; Abdalla, 2017; Davis and Grill, 2018)
The present study showed that microinjection of 0.5 or 5 μg of orexin-A into the central nucleus of the amygdala (CeA) did not significantly affect chow food intake, but significantly increased palatable high fat food intake
The results showed that vagotomy abolished the effects of orexin-A, which supported our hypothesis that orexin-A injected into the CeA signaled through the dorsal motor nucleus of the vagus (DMV), and descending conduction was mediated by vagal nerves
Summary
Food intake is regulated by several interrelated brain regions, including the hypothalamus, the hindbrain, and the limbic system (Merali et al, 2013; Abdalla, 2017; Davis and Grill, 2018). Recent studies showed that the amygdala can integrate feeding-related signals from the cortex, the hypothalamus, and the hindbrain to regulate food intake Projections from the CeA may reach the feeding-related centers in the hypothalamus and/or the hindbrain, the exact neural pathways that control feeding behavior require further study. Anatomical and physiological studies have shown that connections between the CeA and the dorsal vagal complex (DVC), which is a regulatory center for visceral function, affect gastric motility (Liubashina et al, 2000; Zhang et al, 2003; Cassidy et al, 2019)
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