Opioid and α2 adrenergic mechanisms are activated by GABA agonists in the lateral parabrachial nucleus to induce sodium intake.
Brain Res Bull
; 139: 174-181, 2018 05.
Article
em En
| MEDLINE
| ID: mdl-29432796
ABSTRACT
The activation of GABA, opioid or α2 adrenergic mechanisms in the lateral parabrachial nucleus (LPBN) facilitates hypertonic NaCl intake in rats. In the present study, we combined opioid or α2 adrenergic antagonists with GABA agonists into the LPBN in order to investigate if NaCl intake caused by GABAergic activation in normohydrated rats depends on opioid or α2-adrenergic mechanisms in this area. Male Holtzman rats with stainless steel cannulas implanted bilaterally in the LPBN were used. Bilateral injections of muscimol or baclofen (GABAA and GABAB agonists, respectively, 0.5â¯nmol/0.2⯵l) into the LPBN induced strong ingestion of 0.3â¯M NaCl (45.8⯱â¯7.3 and 21.8⯱â¯4.8â¯ml/240â¯min, respectively) and water intake (22.7⯱â¯3.4 and 6.6⯱â¯2.5â¯ml/240â¯min, respectively). Naloxone (opioid antagonist, 150â¯nmol/0.2⯵l) into the LPBN abolished 0.3â¯M NaCl and water intake to muscimol (2.0⯱â¯0.6 and 0.9⯱â¯0.2â¯ml/240â¯min, respectively) or baclofen (2.3⯱â¯1.1 and 0.8⯱â¯0.4â¯ml/240â¯min, respectively). RX 821002 (α2 adrenoceptor antagonist, 10â¯nmol/0.2⯵l) into the LPBN reduced 0.3â¯M NaCl intake induced by the injections of muscimol or baclofen (26.6⯱â¯8.0 and 10.1⯱â¯4.9â¯ml/240â¯min, respectively). RX 821002 reduced water intake induced by muscimol (7.7⯱â¯2.9â¯ml/240â¯min), not by baclofen. The results suggest that sodium intake caused by gabaergic activation in the LPBN in normohydrated rats is totally dependent on the activation of opioid mechanisms and partially dependent on the activation of α2 adrenergic mechanisms in the LPBN.
Palavras-chave
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Sódio
/
Receptores Adrenérgicos alfa 2
/
Agonistas GABAérgicos
/
Núcleos Parabraquiais
/
Analgésicos Opioides
Limite:
Animals
Idioma:
En
Revista:
Brain Res Bull
Ano de publicação:
2018
Tipo de documento:
Article