ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2025
Knockdown of the type 1 cannabinoid receptor in the central amygdala increases both spontaneous and water deprivation-induced sodium intake in rats.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Important inputs originating in the forebrain circumventricular organs and also in the central amygdala (CeA) trigger essential water deprivation (WD)-induced behaviors, such as thirst and sodium appetite. Together with the secretion of the neurohypophysial peptides arginine vasopressin (AVP) and oxytocin (OT), these behavioral responses seek to maintain the normalcy of extracellular fluid (ECF) osmolality and volume. Within this context, the main hypothesis tested by the present study was that CeA type 1 cannabinoid receptors (CB1Rs) were essential for the maintenance of body fluid homeostasis, particularly in response to WD challenge. We found that CeA CB1R knockdown increased spontaneous and WD-induced hypertonic saline intake, without significantly impacting water ingestion. In euhydrated rats, despite unaltered urinary volume, CB1R knockdown reduced urinary osmolality, and diminished urinary nitrate concentrations, suggesting reduced renal sodium excretion. No relevant changes were induced by CeA CB1R knockdown on urinary parameters following WD-induced rehydration, which is consistent with unaltered AVP and OT mRNA transcription and hormone release under the same experimental conditions. Taken together, the present data support the notion that CeA CB1Rs participate in both spontaneous and WD-induced NaCl intake, without significantly affecting neuroendocrine output. Given the well-described facilitatory CeA role on natriorexigenic responses, and the reported interplay between CB1Rs and γ-aminobutyric acid (GABA) within the CeA, the present findings suggest that CB1Rs may indirectly regulate sodium appetite through effects on CeA GABAergic neurotransmission.
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