Inhibitory effect of activation of GABAA receptor in the central nucleus of amygdala on the sodium intake in the sodium-depleted rat

Importance of the central nucleus of the amygdala on sodium intake caused by deactivation of lateral parabrachial nucleus

“…Therefore, the marked ingestion of water in rats treated with muscimol or moxonidine into the LPBN combined with saline into the CeA is probably a consequence of the increased plasma osmolarity due to the simultaneous excessive ingestion of hypertonic NaCl. In this case, the reduced ingestion of water caused by the injections of muscimol into the CeA is probably due to the reduced ingestion of hypertonic NaCl, similar to what was proposed previously for electrolytic lesions of the CeA (Galaverna et al, 1992;Wang et al, 2012;Zardetto-Smith et al, 1994). The inactivation of the CeA with injections of muscimol increases the exploratory behavior in rats (Moreira et al, 2007), which suggests that the effects of muscimol injections into the CeA on water and sodium intake are not due to an impairment of motor activity.…”

“…The anatomical specificity of the LPBN and CeA as the central sites where moxonidine and/or muscimol injections produce effects on water and/or NaCl intake was demonstrated by previous studies (Andrade et al, 2004, Callera et al, 2005Wang et al, 2012). The present results show that muscimol injected outside of the CeA at the dose of 0.25 nmol did not abolish NaCl intake in rats treated with moxonidine into the LPBN, whereas at the dose of 0.5 nmol it blocked NaCl intake in rats treated with muscimol into the LPBN.…”

“…The injections of muscimol into the CeA (present results) similar to electrolytic lesions of the CeA (Andrade-Franze et al, 2010a) produced a tendency to reduce FUROþCAP-induced 0.3 M NaCl intake in rats treated with vehicle into the LPBN. The same treatments in the CeA reduced 0.3 M NaCl intake produced by 24 h of sodium depletion (furosemide followed by 24 h sodium deficient diet) (Galaverna et al, 1992;Wang et al, 2012), which suggests that the facilitatory mechanisms of the CeA are involved in mediating sodium intake in sodium-depleted rats. The low amount of 0.3 M NaCl ingested and the variability of 0.3 M NaCl intake by rats treated with FUROþCAP may explain the absence of significant reduction of 0.3 M NaCl intake in FUROþCAP treated rats that received muscimol into the CeA.…”

AT1 receptor blockade in the central nucleus of the amygdala attenuates the effects of muscimol on sodium and water intake

“…Lately, our laboratory has also demonstrated that the blockade of CeA neurons with bilateral injections of the GABA A receptor agonist muscimol inhibits the ingestion of hypertonic NaCl and water in sodium-depleted rats. This suggests that GABAergic mechanisms present in the CeA are involved in the control of sodium intake (Wang et al, 2012 The cardiovascular, neuroendocrine and ingestive effects of ANG II are mainly mediated by angiotensin II type-1 (AT1) receptors (Kirby et al, 1992;Thunhorst and Fitts, 1994;McKinley et al, 1996;Fitzsimons, 1998). The CeA contains AT1 receptors (Thunhorst and Fitts, 1994;McKinley et al, 1996) and has been proposed as a possible site of interaction between ANG II and mineralocorticoids to stimulate sodium appetite (Galaverna et al, 1992;McKinley et al, 2003).…”

“…Considering the effects of the activation of GABA A receptors in the CeA on hypertonic NaCl and water intake (Kang et al, 2004;Wang et al, 2012), and the already-reported role of AT1 receptor activation in the modulation of GABAergic mechanisms (Li et al, 2003;Li and Pan, 2005;Henry et al, 2009;Xing et al, 2009), in the present study we investigated the effects of previous injection of the specific AT1 receptor antagonist, losartan, into the CeA on water and hypertonic NaCl intake reduced by muscimol injections into the CeA in water deprivation-partial rehydration (WD-PR) or FURO-treated rats.…”