RESUMO
Facilitatory and inhibitory mechanisms in the central nucleus of the amygdala (CeA) and the lateral parabrachial nucleus (LPBN), respectively, are important for the control of sodium and water intake. Here we investigated the importance of the opioid mechanisms in the CeA for water and 0.3M NaCl intake in euhydrated or hyperosmotic rats treated with injections of muscimol (GABAA agonist) or moxonidine (α2 adrenergic/imidazoline agonist) into the LPBN, respectively. Male Holtzman rats (n=4-8/group) with stainless steel cannulas implanted bilaterally in the CeA and in the LPBN were used. The ingestion of 0.3M NaCl and water by euhydrated rats treated with muscimol (0.5nmol/0.2µl) into the LPBN (29.4±2.7 and 15.0±2.4ml/4h, respectively) was abolished by the previous injections of naloxone (opioid antagonist, 40µg/0.2µl) into the CeA (0.7±0.3 and 0.3±0.1ml/4h, respectively). The ingestion of 0.3M NaCl by rats treated with intragastric 2M NaCl (2ml/rat) combined with moxonidine (0.5nmol/0.2µl) into the LPBN (17.0±3.8ml/2h) was also strongly reduced by the previous injections of naloxone into the CeA (3.2±2.5ml/2h). Sucrose intake was not affected by naloxone injections into the CeA, which minimized the possibility of non-specific inhibition of ingestive behaviors with this treatment. The present results suggest that opioid mechanisms in the CeA are essential for hypertonic NaCl intake when the LPBN inhibitory mechanisms are deactivated or attenuated with injections of muscimol or moxonidine in this area.
Assuntos
Analgésicos Opioides/metabolismo , Núcleo Central da Amígdala/fisiologia , Vias Neurais/fisiologia , Núcleos Parabraquiais/fisiologia , Sódio/metabolismo , Animais , Anti-Hipertensivos/farmacologia , Núcleo Central da Amígdala/efeitos dos fármacos , Ingestão de Líquidos/efeitos dos fármacos , Ingestão de Líquidos/fisiologia , Agonistas de Receptores de GABA-A/farmacologia , Imidazóis/farmacologia , Masculino , Muscimol/farmacologia , Naloxona/farmacologia , Antagonistas de Entorpecentes/farmacologia , Vias Neurais/efeitos dos fármacos , Núcleos Parabraquiais/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Sódio na DietaRESUMO
The lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important central areas for the control of sodium appetite. In the present study, we investigated the importance of the facilitatory mechanisms of the CeA on NaCl and water intake produced by the deactivation of LPBN inhibitory mechanisms. Male Holtzman rats (n=7-14) with stainless steel cannulas implanted bilaterally in the CeA and LPBN were used. Bilateral injections of moxonidine (α2-adrenoceptor/imidazoline agonist, 0.5 nmol/0.2 µl) into the LPBN increased furosemide+captopril-induced 0.3M NaCl (29.7 ± 7.2, vs. vehicle: 4.4 ± 1.6 ml/2h) and water intake (26.4 ± 6.7, vs. vehicle: 8.2 ± 1.6 ml/2h). The GABAA agonist muscimol (0.25 nmol/0.2 µl) injected bilaterally into the CeA abolished the effects of moxonidine into the LPBN on 0.3M NaCl (2.8 ± 1.6 ml/2h) and water intake (3.3 ± 2.3 ml/2h). Euhydrated rats treated with muscimol (0.5 nmol/0.2 µl) into the LPBN also ingested 0.3M NaCl (19.1 ± 6.4 ml/4h) and water (8.8 ± 3.2 ml/4h). Muscimol (0.5 nmol/0.2 µl) into the CeA also abolished 0.3M NaCl (0.1 ± 0.04 ml/4h) and water intake (0.1 ± 0.02 ml/4h) in euhydrated treated with muscimol into the LPBN. The present results show that neuronal deactivation of the CeA abolishes NaCl intake produced by the blockade of LPBN inhibitory mechanisms, suggesting an interaction between facilitatory mechanisms of the CeA and inhibitory mechanisms of the LPBN in the control of NaCl intake.
Assuntos
Núcleo Central da Amígdala/fisiologia , Comportamento de Ingestão de Líquido/efeitos dos fármacos , Núcleos Parabraquiais/fisiologia , Sódio/metabolismo , Animais , Anti-Hipertensivos/farmacologia , Captopril/farmacologia , Núcleo Central da Amígdala/efeitos dos fármacos , Ingestão de Líquidos/efeitos dos fármacos , Furosemida/farmacologia , Agonistas de Receptores de GABA-A/farmacologia , Imidazóis/farmacologia , Masculino , Muscimol/farmacologia , Vias Neurais/efeitos dos fármacos , Vias Neurais/fisiologia , Ratos , Ratos Sprague-Dawley , Inibidores de Simportadores de Cloreto de Sódio e Potássio/farmacologia , Fatores de TempoRESUMO
Bilateral injections of moxonidine, an α2-adrenoceptor and imidazoline receptor agonist, into the lateral parabrachial nuclei (LPBN) enhance sodium appetite induced by extracellular dehydration. In the present study, we examined whether LPBN moxonidine treatments change taste reactivity to hypertonic NaCl solution administered into the mouth by intra-oral (IO) cannula. Male Holtzman rats prepared with IO and bilateral LPBN cannulas received subcutaneous injections of furosemide (FURO; 10 mg/kg) and captopril (CAP; 5 mg/kg) to induce hypovolemia with mild hypotension and an accompanying salt appetite and thirst before testing the taste reactivity to oral infusions of 0.3 M NaCl (1.0 ml/min). In the first experiment 45 min after subcutaneous injections of FURO+CAP or vehicle, moxonidine was bilaterally injected into the LPBN, and then 15 min later both bodily and oral-facial ingestive and rejection responses to 0.3 M NaCl delivered through the IO cannula were assessed. Both LPBN vehicle and moxonidine treated rats showed increased ingestive and decreased rejection responses to the IO hypertonic solution. The IO 0.3 M NaCl infusion-evoked ingestive and rejection taste related behaviors were comparable in the LPBN vehicle- vs. the LPBN moxonidine-injected groups. In a second experiment, rats received the same FURO+CAP treatments and LPBN injections. However, beginning 15 min after the LPBN injections, they were given access to water and 0.3M NaCl and were allowed to consume the fluids for most of the next 60 min with the free access intake being interrupted only for a few minutes at 15, 30 and 60 min after the fluids became available. During each of these three brief periods, a taste reactivity test was conducted. On the three taste reactivity tests rats that received LPBN vehicle injections showed progressive declines in ingestive responses and gradual increases in rejection responses. However, in contrast to the LPBN vehicle treated rats, animals receiving bilateral injections of LPBN moxonidine maintained a high number of ingestive responses and a low number of rejection responses throughout the test period even in spite of evidencing substantial water and 0.3 M NaCl consumption during the periods of free access. The results suggest that after α2-adrenoceptor agonist delivery to the LPBN the acceptance of 0.3 M NaCl is sustained and the negative attributes of the solution are minimized. The maintained positive rewarding qualities of 0.3 M NaCl are likely to account for why LPBN moxonidine treated rats show such a remarkable salt appetite when assayed by the volume of hypertonic 0.3 M NaCl consumed.
Assuntos
Agonistas Adrenérgicos/farmacologia , Imidazóis/farmacologia , Ponte/efeitos dos fármacos , Solução Salina Hipertônica/administração & dosagem , Paladar/efeitos dos fármacos , Animais , Anti-Hipertensivos/farmacologia , Captopril/farmacologia , Diuréticos/farmacologia , Comportamento de Ingestão de Líquido/efeitos dos fármacos , Vias de Administração de Medicamentos , Interações Medicamentosas , Furosemida/farmacologia , Masculino , Ponte/fisiologia , Ratos , Fatores de TempoRESUMO
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.