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Antidepressant agents have been associated with gynecomastia, but evidence for a causal link is insufficient.
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Venlafaxine (VEN), a serotonin and noradrenaline reuptake inhibitor is being used as a drug of choice for treating clinical depression even during pregnancy. It is an important therapeutic option in the treatment of perinatal depression, but the effects of VEN on fetus and the newborn are uncertain. Therefore, present study was undertaken to investigate the safety of in-utero exposure to VEN in terms of developmental neurotoxicity and neurodegenerative potential by using prenatal rat model. The selected doses of VEN (25, 40 and 50mg/kg) were administered to pregnant rats from GD 5 to 19 through oral gavage. The fetal brains were dissected and processed for histopathological measurements of neocortical thickness that showed significant reduction. Considering vulnerability of immature brain to free radical injury, VEN exposed neocortices were tested for reactive oxygen species (ROS) levels which were significantly increased. As ROS play important role in the initiation of apoptotic mechanisms, we explored for in situ detection of apoptosis by confocal microscopy that showed enhanced apoptosis including chromatin condensation which was further reconfirmed by electron microscopy. Substantially increased levels of pro-apoptotic protein Bax and decreased levels of anti-apoptotic protein Bcl2 as shown by western blotting also supported the increased neuro-apoptotic degeneration. For further correlation of these findings, prenatally VEN exposed young-adult rat offspring were assessed for open field exploratory behavior that showed increased anxiety-like and stereotypic responses indicating disturbed neurobehavioral pattern. The study concludes that prenatal VEN exposure may primarily enhance ROS generation that plays a key role in regulating release of proapoptotic factors from mitochondria and thereby enhancing apoptotic neurodegeneration that affect proliferation, migration and differentiation of cells, resulting in neuronal deficits manifested as long term neurobehavioral impairments.
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Venlafaxine hydrochloride, a structurally novel antidepressant, is also the first nontricyclic serotonin/norepinephrine reuptake inhibitor. Although venlafaxine has an overall side effect and safety profile that is comparable to other newer antidepressants, it can cause both transient and sustained elevations of supine diastolic blood pressure (SDBP), probably the result of noradrenergic potentiation.
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To evaluate the efficacy, safety, and tolerability of flexible-dose venlafaxine ER compared with placebo in the short-term treatment of generalized social anxiety disorder and, secondarily, to compare paroxetine with venlafaxine ER and paroxetine with placebo.
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Case report and literature review.
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This study was performed on rats after chronic constriction injury (CCI) to the sciatic nerve. The von Frey and Hargreaves' tests were used to assess mechanical allodynia and thermal hyperalgesia, respectively, after intraplantar (ipl) or subcutaneous (sc) administration of amitriptyline, doxepin, or venlafaxine, or their ipl co-administration with morphine on day 12-16 after injury.
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Amitriptyline up-regulated SOD1 messenger RNA in a time- and dose-dependent manner. The greatest up-regulation was following incubation with 10 mumol/L amitriptyline for 48 hours. The addition of bupropion, doxepin or venlafaxine to PC12 cell cultures also up-regulated SOD1 mRNA.
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Nearly 70% of participants had anxious depression. Remission rates were significantly lower and ratings of adverse event frequency were significantly greater in patients with anxious TRD than in those with nonanxious TRD. Presence of anxious depression predicted worse outcomes.
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Heart rate variability (HRV) reflects the cardiac autonomic regulation, and reduced HRV is considered a pathophysiological link between depression and cardiovascular mortality. So far, there is only limited information on the effects of venlafaxine and mirtazapine on HRV.We studied 28 nondepressed controls and 41 moderately depressed patients being treated with venlafaxine (n = 20) and mirtazapine (n = 21). Heart rate, blood pressure, and HRV were measured after a 6-day washout as well as after 14 and 28 days of treatment in supine and upright position.We found increased heart rate and reduced HRV in the depressed patients compared with the nondepressed controls. Moreover, HRV total power declined during the treatment period. Medication and remission status after 4 weeks were not related to the change in HRV.We conclude that depression is related to reduced HRV, which might reflect sympathovagal dysbalance. The widely used antidepressants venlafaxine and mirtazapine led to further decline in HRV. Clinicians should consider HRV effects in the selection of antidepressants.