RESUMEN
The effects of icv administration of beta-endorphin on secretory activity of dopaminergic neurons is described. Homovanillic and dihydroxyphenyl acetic acid levels in cerebrospinal fluid and extracts of brain tissue were determined after administration of beta-endorphin to animals pretreated or not with naloxone. The results suggest that beta-endorphin interferes with formation of dopaminergic metabolites by acting on opioid receptors.
Asunto(s)
Ácido 3,4-Dihidroxifenilacético/líquido cefalorraquídeo , Cuerpo Estriado/metabolismo , Ácido Homovanílico/líquido cefalorraquídeo , Fenilacetatos/líquido cefalorraquídeo , Sustancia Negra/metabolismo , betaendorfina/fisiología , Animales , Dopamina/metabolismo , Naloxona/uso terapéutico , Neuronas/fisiología , RatasRESUMEN
Epidemiologic and pharmacologic evidence suggests that abnormalities of catecholaminergic systems in the brain play a role in the pathogenesis of minimal brain dysfunction, but previous attempts to document a neurochemical abnormality have been unsuccessful. To better define central nervous system mechanisms in children with MBD, we have utilized the probenecid loading technique to determine the concentrations of metabolites in the CSF of a clinically homogeneous group of children with MBD. CSF concentrations of homovanillic acid, the principal metabolite of dopamine, correlated directly with CSF probenecid in 26 control subjects (r = 0.05, p less than 0.01) and in six children with MBD (r = 0.91, p less than 0.05). Concentration of HVA (ng/ml) per unit of probenecid (mug/ml) was found to be significantly lower in children with MBD (9.8 +/- 1.5, mean +/- SEM) compared to those in control subjects (16.5 +/- 1.5), suggesting reduced turnover of brain dopamine in the MBD group. CSF concentrations of 5-hydroxyindoleacetic acid (5-HIAA), the principle metabolite of serotonin, did not differ significantly between the groups. Our findings indicate that there may be a neurochemical abnormality in MBD.