RESUMO
Catabolism of 5-hydroxytryptamine in the midbrain raphe nuclei of aggressive C57Bl/6J mice increased after 10 and 20 days of confrontations. Both catabolism and concentration of 5-hydroxytryptamine increased in the dopaminergic nuclei A11, A10, A9, and in the amygdala. The level of 5-hydroxyindoleacetic acid in the A9 and raphe nuclei decreased after 20 days of confrontations, which coincided with manifestation of the immune response.
Assuntos
Agressão/fisiologia , Encéfalo/metabolismo , Ácido Hidroxi-Indolacético/metabolismo , Camundongos Endogâmicos C57BL/imunologia , Serotonina/metabolismo , Animais , Ácido Hidroxi-Indolacético/análise , Imunização , Camundongos , Serotonina/análise , Ovinos , Baço/imunologiaRESUMO
Changes in the reactivating efficiency of blockade of components of the GABA-benzodiazepine-ionophore complex were analyzed in conditions of preliminary activation and inhibition of dopamine autoreceptors using (+)ZRRR and haloperidol respectively. A conditioned passive escape reflex was used, along with amnesia produced by detaining mice in the danger sector of a chamber immediately after imposition of a painful stimulus. Doses of bicuculline (1 mg/kg), picrotoxin (1 mg/kg), and flumazenil (10 mg/kg) given before testing restored performance of the conditioned response without altering the neurochemical background. Reductions and increases in dopaminergic activity during the training period prevented restoration of the conditioned passive escape response by blockade of GABAa and benzodiazepine receptors and chloride channels. It is suggested that the neurochemical mechanisms involved in restoring the damaged memory trace are based on the formation of te optimal balance in the activities of the various components of the GABA-benzodiazepine-ionophore complex and the dopaminergic system.
