Lesions in the central amygdala impair sodium intake induced by the blockade of the lateral parabrachial nucleus

Abstract

The blockade of the lateral parabrachial nucleus (LPBN) with the GABAergic receptor agonist muscimol induces strong hypertonic NaCl intake in satiated and normovolemic rats, whereas lesions of the central nucleus of the amygdala (CeA) reduce sodium intake induced by different protocols. In the present study we investigated the effects of bilateral lesions of the CeA on water and 0.3M NaCl intake induced by GABAergic receptor activation with bilateral injections of muscimol into the LPBN in satiated rats. Male Holtzman rats (n=6-10) with bilateral sham or electrolytic lesions (2mA; 10s) of the CeA and stainless steel cannulas implanted bilaterally in the LPBN were used. Bilateral injections of muscimol (0.5nmol/0.2microl) into the LPBN in satiated sham-lesioned rats induced 0.3M NaCl intake (16.1+/-5.4ml/4h, vs. saline: 1.3+/-0.5ml/4h) and water intake (8.1+/-3.5ml/4h, vs. saline: 1.6+/-0.5ml/4h). Bilateral lesions of the CeA (3days) abolished 0.3M NaCl intake (0.1+/-0.1ml/4h) and water intake (0.1+/-0.1ml/4h) induced by bilateral injections of muscimol into the LPBN in satiated rats. The present results show that water and 0.3M NaCl intake induced by the blockade of LPBN neurons with muscimol depends on the integrity of the CeA, suggesting that facilitatory mechanisms present in the CeA are essential for water and hypertonic NaCl intake that arises after the blockade of the inhibitory mechanisms of the LPBN with muscimol.

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

“…Furthermore, bilateral electrolytic lesions of the CeA abolish water and 0.3 M NaCl intake produced by bilateral injections of the GABA A agonist muscimol into the LPBN in normovolemic and euhydrated rats (Andrade-Franze et al, 2010a). These results suggest that the integrity of the CeA is essential for sodium intake that results from the deactivation of the LPBN inhibitory mechanisms (Andrade-Franze et al, 2010a, 2010b.…”

“…The LPBN strongly inhibits hypertonic NaCl intake, an influence which is hypothesized to prevent excessive solute intake (Andrade-Franze et al, 2010a, 2010bAndrade et al, 2004Andrade et al, , 2011Callera et al, 2005;De Oliveira et al, 2008;Gasparini et al, 2015a;Menani et al, 2014;Roncari et al, 2014). Signals that influence water and NaCl intake like those from arterial baroreceptors, cardiopulmonary receptors, gustatory receptors and other visceral receptors that reach the NTS ascend to the LPBN (Norgren, 1981;Lança and van der Kooy, 1985;Ciriello et al, 1984;Fulwiler and Saper, 1984;Herbert et al 1990;Jhamandas et al, 1992Jhamandas et al, , 1996.…”

“…The FUROþCAP is a treatment that induces hypovolemia, mild hypotension and acute NaCl and water intake dependent on central production of angiotensin II (ANG II) (Andrade et al, 2004;Fitts and Masson, 1989;Gasparini et al, 2009;Thunhorst and Johnson, 1994). Furthermore, bilateral electrolytic lesions of the CeA abolish water and 0.3 M NaCl intake produced by bilateral injections of the GABA A agonist muscimol into the LPBN in normovolemic and euhydrated rats (Andrade-Franze et al, 2010a). These results suggest that the integrity of the CeA is essential for sodium intake that results from the deactivation of the LPBN inhibitory mechanisms (Andrade-Franze et al, 2010a, 2010b.…”

Activation of μ opioid receptors in the LPBN facilitates sodium intake in rats

“…Bilateral electrolytic lesions of the CeA blocked the increase of NaCl intake induced by injections of moxonidine (␣ 2 -adrenoceptor/imidazoline receptor agonist) or methysergide (serotonergic receptor antagonist) into the LPBN in FURO + CAP-treated rats [47]. The ingestion of NaCl induced by the GABA A receptor agonist muscimol injected into the LPBN is also abolished by lesions of the CeA [48]. These results suggest an interaction between the facilitatory mechanisms for sodium intake present in the CeA with the inhibitory mechanisms of the LPBN.…”

Characterizing the neuropeptide pathways between the forebrain and the pons.

“…Indeed, GABA has been shown to produce a concentration-dependent reduction in input resistance of neurons in the caudomedial gustatory zone of the PBN (Kobashi and Bradley, 1998). Blockade of activity in the PBN with the GABAergic receptor agonist muscimol induces strong hypertonic NaCl intake that is dependent upon the integrity of the CeA (ndrade-Franze et al, 2010). Moreover, enhancement of PBN GABA neurotransmission via midazolam microinjection increased food intake and selectively enhanced positive behavioral reactions to oral infusion of solutions containing bitter and sweet compounds (Soderpalm and Berridge, 2000).…”