ACTIVATION OF ji-OPIOID RECEPTORS IN THE CENTRAL NUCLEUS OF THE AMYGDALA INDUCES HYPERTONIC SODIUM INTAKE

摘要

Sodium (Na+), as the most abundant electrolyte in the extracellular fluid (ECF) compartment, plays a critical role in maintaining hydromineral and cardiovascular homeostasis. Na+ hunger, which is also known as salt appetite, is a goal-directed behavior that arises in rodents and other species in specific response to volume and/or Na+ depletion in the ECF compartment (Weisinger et al., 1979; Johnson and Thunhorst, 1997). The amygdala, a brain structure containing distinct nuclei, influences a great number of behaviors tailored to promote the animal's adaptation to external and internal stimuli (Price et al., 1987), and has been believed to participate in the regulation of sodium intake (Covian et al., 1975; Galaverna et al., 1992; Zhang et al., 1993; Zardetto-Smith et al., 1994; Swanson and Petrovich, 1998; Johnson et al., 1999). The distinct nuclei within the amygdala may play specific functional roles in the control of salt intake. Surgical lesions of the basolateral amygdala (BLA) inhibit salt intake induced by mineralocorticoid treatment (Nachman and Ashe, 1974). Lesions of the medial amygdala (MeA) impair mineralocorticoid-induced salt intake but do not affect salt intake promoted by sodium depletion (Nitabach et al., 1989; Zhang et al., 1993). Different studies have also shown the importance of the central nucleus of the amygdala (CeA) in the control of the ingestion of sodium intake. Bilateral electrolytic lesions of the CeA reduce spontaneous sodium intake, as well as sodium appetite induced by subcutaneous injections of the mineralocorticoid deoxycorticosterone, the oc2-adrenoceptor antagonist yohimbine, or angiotensin II (ANG II), intracerebral ventricle injections of renin or by 24 h of sodium depletion in rats treated with furosemide (Galaverna et al., 1992; Zardetto-Smith et al., 1994).