Baclofen into the lateral parabrachial nucleus induces hypertonic sodium chloride and sucrose intake in rats.

Abstract

GABAA and GABAB receptors are present in the lateral parabrachial nucleus (LPBN), a pontine area involved with inhibitory mechanisms related to the control of sodium appetite. Activation of GABAA receptors in the LPBN induces strong ingestion of 0.3 M sodium chloride (NaCl) in normonatremic and euhydrated rats. In the present study, we investigated the effects of the GABAB receptor agonist baclofen, injected alone or combined with GABAA or GABAB receptor antagonists into the LPBN on 0.3 M NaCl, water, 0.06 M sucrose and food intake in normonatremic and euhydrated rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally in the LPBN were used. In normonatremic and euhydrated rats, bilateral injections of baclofen (0.5 nmol/0.2 _l) into the LPBN induced 0.3 M NaCl (24.0_3.1 vs. saline: 2.0_0.8 ml/240 min) and water intake (10.6_1.4 vs. saline: 3.5_0.7 ml/240 min) in a two-bottle test. Injections of GABAB receptor antagonists CGP 35348 (50 nmol/0.2 _l) or 2-hydroxysaclofen (5 nmol/0.2 _l) or GABAA receptor antagonist bicuculline (1.6 nmol/0.2 _l) into the LPBN reduced 0.3 M NaCl (14.1_4.7 ml/240 min; 9.97_2.5 ml/210 min; 8.8_5.9 ml/240 min, respectively) and water intake induced by baclofen injected into the LPBN. Baclofen (0.5 nmol/0.2 _l) injected into the LPBN also induced 0.06 M sucrose intake (21.8_5.9 vs. saline: 5.0_2.6 ml/180 min). Urinary volume and sodium excretion had a tendency to decrease after baclofen injection into the LPBN, whereas arterial pressure and food intake were not affected. The results show that baclofen injected into the LPBN, in normonatremic and euhydrated rats, produces a natriorexigenic effect dependent on GABAA and GABAB receptor activation. The natriorexigenic effect is not secondary to alterations in blood pressure or sodium urinary excretion. In addition, baclofen injected into the LPBN also induces 0.06 M sucrose intake.