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Valsartan hexal 160 mg preis oprodol 100 preluminal preparation 3.5 mg/kg or 5 g/kg for treatment of major depression. [13] Phenobarbital (25 mg/kg, i.p.) in rats following tricyclic antidepressants was found to have no effect on hippocampal 5-HT and noradrenaline uptake [58]. A reduction of cerebral 5-HT uptake was found in rats given the combination of carbamazepine and imipramine (10 mg/kg, i.p.) for 7 days without a concomitant antidepressant treatment and imipramine (10 mg/kg, i.p.) with carbamazepine (0.5 for 7 days [59]. Golimumab and imipenem were both found not to alter either cortical or hippocampal 5-HT uptake. Imipenem (4 mg/kg, i.p.) but not golimumab (1 mg/kg, i.p.) affected 5-HT uptake [60]. Gibberellin A was found not to affect either cortical or hippocampal 5-HT uptake in adult rats [61]. A reduction in hippocampal 5-HT uptake was found following repeated or chronic administration of haloperidol (1 mg/kg, i.p.) and memantine (10 alone [62]. An increase in hippocampal 5-HT uptake was found following repeated or chronic administration of olanzapine (1 mg/kg, i.p.) with haloperidol but not in the absence of olanzapine [63]. The effect of imipramine (1 mg/kg, i.p.) on hippocampal 5-HT uptake was not different from that of imipramine alone [64]. Administration of imipramine (1 mg/kg, i.p.) alone increased 5-HT uptake but not 5-HIAA levels in hippocampus and cortex of rats [65]. Subchronic imipramine administration in rats resulted an induction of 5-HT release from rat hippocampus and cortical areas [66]. The effect of imipramine (1 mg/kg, i.p.) administration on 5-HT uptake was found to be dose-dependent and abolished by atropine, a 5-HT releaser [67]. Administration of imipramine (1 mg/kg, i.p.) in rats led to a dose-dependent increase in hippocampal 5-HT release (0.1–5.0 mg/kg) [68]. A dose-dependent increase in rat cortical 5-HT release was found following imipramine (100 mg/kg, i.p.) administration in rats [69]. Subchronic administration of imipramine in rats led to a dose-dependent increase in hippocampal and cortical 5-HT release after 5 days [70]. A dose-dependent increase in rat cortical 5-HT release was found following imipramine (1 mg/kg, i.p.) administration in rats [71]. Subchronic administration of imipramine in rats led to a dose-dependent increase in rat hippocampal 5-HT release [72]. Subchronic imipramine administration (10 mg/kg, i.p.) led to an increase in rat cortical 5-HT release [73]. Subchronic imipramine (10 mg/kg, i.p.) administration appeared to increase the magnitude of in cortical 5-HT release rats [40]. Subchronic imipramine (10 mg/kg, i.p.) administration increased the magnitude of increase in animal 5-HT release compared to the non-imipramine (control) group [74]. Administration of imipramine (50 mg/kg, i.p.) resulted in a dose-dependent increase cortical 5-HT release from rat hippocampus [75]. Subchronic imipramine (50 mg/kg, i.p.) or plus gabapentin (30 mg/kg, i.p.) administration led to a dose-dependent increase in rat cortical 5-HT release [76]. Administration of imipramine (25 mg/kg, i.p.) in mice resulted a dose-dependent increase in hippocampal 5-HT release [77]. Subchronic imipramine (50 mg/kg, i.p.) but not imipramine plus g.
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