ESTRADIOL DECREASES REACTIVE ASTROGLIOSIS AFTER BRAIN INJURY BY A MECHANISM INVOLVING THE ENDOCANNABINOID SYSTEM.

LÓPEZ RODRÍGUEZ AB; MATEOS VICENTE B; ROMERO-ZERBO SY; RODRIGUEZ-RODRIGUEZ N; BELLINI MJ; RODRIGUEZ DE FONSECA F; BERMUDEZ-SILVA FJ; AZCOITIA I; GARCIA-SEGURA LM; VIVEROS MP

Málaga, España

Otro; V Reunión de la Red Glial Española; 2010

The neuroactive steroid estradiol reduces reactive astroglia after brain injury bymechanisms similar to those involved in the regulation of reactive gliosis byendocannabinoids. In this study we have explored whether cannabinoid receptorsare involved ¡n the effects of estradiol on reactive astroglia. To test this hypothesis,the effects of estradiol, the cannabinoid CBi antagonist / inverse agonist AM251and the cannabinoid CB2 antagonist / inverse agonist AM630 were assessed ¡n thecerebral cortex of male rats after a stab wound brain injury. Estradiol reduced thenumber of vimentin immunoreactive astrocytes and the number of glial fibrillaryacidic protein immunoreactive astrocytes ¡n the proximity of the wound. The effect ofestradiol was significantly inhibited by the administration of either CB-i or 662receptor antagonists. The effect of estradiol may be in part mediated by alterationsin endocannabinoid signaling, because the hormone increased ¡n the injuredcerebral cortex the mRNA levéis of CB2 receptors and of some of the enzymesinvolved in the synthesis and metabolism of endocannabinoids. These findingssuggest that estradiol may decrease reactive astroglia in the injured brain byregulating the activity of the endocannabinoid system.