Effect of electroconvulsive shock on serotonin activity.
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Biomedical subjects
Publications and source records attributed to W B Essman.
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Aging mice showed a retrograde amnesia for passive avoidance behavior when a single electroconvulsive shock (ECS) was given at post-training intervals up to 1 h, whereas adult mice showed no significant amnesia when ECS was given 10 min or more after training. Catecholamines (norepinephrine and dopamine), but not serotonin (5-HT) changed with aging in the several brain regions, but only 5-HT was significantly changed (elevated) by ECS. Protein synthesis was significantly inhibited by ECS, notably in limbic structures. The increased susceptibility of aging mice to the amnesic effect of ECS could be related to aging-related changes in the rate of memory consolidation or to the duration of neural chemical changes that disrupt processes such as consolidation, storage, and/or retrieval of the memory trace.
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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.
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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.
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Mice were exposed to either air or cigarette smoke and the content and uptake of serotonin and activity of monoamine oxidase were determined. Serotonin concentration increased as a function of the frequency of exposure, while serotonin uptake by the skin was maximally increased after two 8 min. exposures. MAO activity for serotonin, but not for tyramine, was decreased by cigarette smoke exposure of more than 8 min.
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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.
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