Chronic Stress Attenuation of a2-Adrenoceptor Reactivity is Reversed by Naltrexone

L. M. CANCELA, M. VOLOSIN AND V. A. MOLINA

PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR

PERGAMON-ELSEVIER SCIENCE LTD

Año: 1988 vol. 31 p. 33 - 35

0091-3057

CANCELA, L. M., M. VOLOSIN AND V. A. MOLINA. Chronic stress attenuation of a~-adrenoceptor reactivity is reversed by naltrexone. PHARMACOL BIOCHEM BEHAV 31(1) 33-35, 1988.--Low doses of clonidine (50-100/zg/kg IP) evoke a clear dose-dependent hypoactivity response. Seven daily immobilization sessions prevented the motor activity decrease induced by clonidine. On the contrary, a single stress failed to modify clonidine response. Pretreatment with naitrexone (2 mg/kg IP) fully antagonized the attenuating effect induced by chronic stress on clonidine sedative action. These evidences suggest that chronic but not acute stress reduces the reactivity of a2-adrenoceptors involved in clonidineinduced sedation. In addition, a regulatory mechanism of endogenous opioids seems to participate on t~2-adrenoceptors adaptative changes.Chronic stress attenuation of a~-adrenoceptor reactivity is reversed by naltrexone. PHARMACOL BIOCHEM BEHAV 31(1) 33-35, 1988.--Low doses of clonidine (50-100/zg/kg IP) evoke a clear dose-dependent hypoactivity response. Seven daily immobilization sessions prevented the motor activity decrease induced by clonidine. On the contrary, a single stress failed to modify clonidine response. Pretreatment with naitrexone (2 mg/kg IP) fully antagonized the attenuating effect induced by chronic stress on clonidine sedative action. These evidences suggest that chronic but not acute stress reduces the reactivity of a2-adrenoceptors involved in clonidineinduced sedation. In addition, a regulatory mechanism of endogenous opioids seems to participate on t~2-adrenoceptors adaptative changes.PHARMACOL BIOCHEM BEHAV 31(1) 33-35, 1988.--Low doses of clonidine (50-100/zg/kg IP) evoke a clear dose-dependent hypoactivity response. Seven daily immobilization sessions prevented the motor activity decrease induced by clonidine. On the contrary, a single stress failed to modify clonidine response. Pretreatment with naitrexone (2 mg/kg IP) fully antagonized the attenuating effect induced by chronic stress on clonidine sedative action. These evidences suggest that chronic but not acute stress reduces the reactivity of a2-adrenoceptors involved in clonidineinduced sedation. In addition, a regulatory mechanism of endogenous opioids seems to participate on t~2-adrenoceptors adaptative changes.