Developmental Variations in CSF Monoamine Metabolites during Childhood

Cerebrospinal (CSF) fluid content of the stable metabolites homovanillic acid, 3-methoxy-4-hydroxyphenyl glycol and 5-hydroxyindoleacetic acid were measured in 19 children without neurological disease known to alter CSF monoamine metabolites. The CSF levels of all three metabolites were found to be up 6 times higher in early infancy compared to the values during adolescence. The levels decreased in a logarithmic fashion, and adult values (approx. 25–50 ng/ml) were reached at 3–5 years of age. Two different interpretations of the findings are discussed: (1) a higher release or turnover of central serotonin and catecholamine metabolites during early postnatal age, or (2) lower clearance of the stable acid metabolites from CSF during infancy due to relatively immature active transport mechanisms.</jats:p

Enhancement of ethanol-induced sedation and hypothermia by centrally administered neurotensin, β-endorphin and bombesin

Intracisternal administration of three endogenous neuropeptides (neurotensin, β-endorphin, or bombesin) potentiated the duration of sedation induced by a fixed dose of ethanol (5.2 g/kg) in mice. The minimally effective dose of each peptide that enhanced ethanol-induced sedation was: neurotensin, 0.18 nmoles; β-endorphin, 1.79 nmoles; and bombesin, 0.06 nmoles. The enhancement of ethanol-induced sedation was correlated with the potentiation of ethanol-induced hypothermia for all three peptides. None of the neuropeptides studied significantly altered blood or brain ethanol concentrations, suggesting that the observed effects were not due to differences in ethanol metabolism