Concentration of 5-hydroxyindoleacetic acid, homovanillic acid, and tryptophan in the cerebrospinal fluid of depressed patients before and after ECT.

Cerebrospinal fluid (CSF) levels of 5-hydroxyindoleacetic acid (5HIAA), tryptophan (TRYP), and homovanillic acid (HVA), were determined prior to electroconvulsive therapy (ECT) and after an average course of 6.7 ECT in six endogenous depressed patients. Depression rating scale (DRS) scores were also obtained by a "blind" research psychiatrist before and after ECT at the time of each lumbar puncture. ECT markedly reduced DRS scores but did not significantly alter CSF levels of 5HIAA, TRYP, or HVA. We found no correlation between ECT-induced DRS score reductions and changes in any of the CSF constituents studied, or between the absolute DRS score and the corresponding CSF concentration of any of the compounds. These data are consistent with those previously reported for ECT and do not suggest that ECT alters cerebral amine metabolism in depressed patients. Neither do they provide any evidence for direct amine mediation of the depression-relieving effects of ECT in man, nor for any relation between severity of depressive illness and CSF concentrations of 5HIAA, TRYP, or HVA.

Histaminergic mediation of the response of rat skin to topical fluorides.

The topical application of sodium fluoride to abraded rat skin produced several morphological and biochemical effects. Related to the degranulation of dermal mast cells, skin histamine concentration was increased, fluorides were absorbed into the skin, and deposited mainly kin mitochondria. Dermal histamine binding was decreased for both H1 and H2 receptors with reduced binding sites, but epidermal adenyl cyclase was activated by fluorides. The response of the rat skin to fluorides involves a sequence of changes by which the potentiation of an inflammatory response also involves alterations in specific histamine receptors and a histamine-specific adenyl cyclase system.

Sex differences in fetal sheep adrenal steroidogenesis.

The formation of several steroids was determined in vitro in adrenals removed from 18 female and six male fetuses of 113-115 days' gestation and in two female and two male fetuses at near term (137-143 days). Samples were incubated with 14C-acetate and the formation of labeled steroids was determined by two-dimensional paper chromatography. Protein and corticosterone concentrations were determined by chromophore absorption and acid hydrolysis fluorescence methods, respectively. Tissue corticosterone concentrations were significantly higher in female (0.145 +/- 0.010 microgram/mg protein) than in male (0.083 +/- 0.010 microgram/mg protein) adrenal tissue at both stages, whereas corticosterone formation was similar in both sexes. Cholesterol formation was significantly higher in female (0.103 +/- 0.079 muM/mg protein) than in male (0.044 +/- 0.011 muM/mg protein) adrenals at both stages. Both testosterone and estradiol were synthesized at higher rates in female than in male adrenals (52% and 33%, respectively), whereas pregnanediol formation was 21% higher in the male. These results indicate that significant sex differences exist in the formation of various adrenocortical hormones by fetal tissues. The relevance of these findings to better survival of female premature newborns from respiratory distress syndrome in contrast with male, is discussed.

Fetal adrenal steroidogenesis: drug effects in sheep.

The influence of ACTH (100 pg/ml), ethanol (10(-3)/M) and morphine (10(-6)/M) on the rate of formation of cholesterol and various steroids in female fetal adrenal tissue was studied in vitro. ACTH and ethanol had no effect on corticosterone formation, while morphine increased it significantly (0.586 +/- 0.049 to 0.799 +/- 0.027 microM/mg protein) (P less than 0.02). Cholesterol formation was increased significantly by ethanol (from 0.103 +/- 0.079 to 0.248 +/- 0.035 microM/mg protein) (P less than 0.01) but not by morphine. Both ethanol and morphine significantly decreased testosterone synthesis (from 0.079 +/- 0.043 to 0.019 +/- 0.002 and 0.006 +/- 0.003 microM/mg protein, respectively) (P less than .01, less than .001). Adrenocortical formation of 17-beta estradiol was similarly attentuated by both ethanol (from 0.372 +/- 0.056 to 0.948 +/- 0.024 microM/mg protein) and morphine (to 0.600 +/- 0.020 microM/mg protein). Adrenocortical pregnanediol formation was significantly decreased by both ethanol (50%; P less than .01) and morphine (36%; P less than .02). Thus, the effect of ethanol and morphine on testosterone, estradiol and pregnanediol was similar and consisted of suppression. The effects of these agents upon corticosterone and cholesterol formation were different. Ethanol, like ACTH, did not stimulate corticosterone formation, but such stimulation did occur with morphine. Ethanol, but not morphine, stimulated cholesterol formation. The data suggest that agents capable of placental transport affect the formation of adrenocortical hormones in the fetal adrenal.