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Neurosci Lett. 2003 May 15;342(1-2):105-8.
The antihyperalgesic effect of venlafaxine in diabetic rats does not involve the opioid system.
Marchand F, Alloui A, Chapuy E, Hernandez A, Pelissier T, Ardid D, Eschalier A.
E 9904 INSERM/UdA, Laboratoire de Pharmacologie Medicale, Faculte de Medecine, 63001 Cedex 1, Clermont-Ferrand, France.
Venlafaxine (VFX) is a structurally novel antidepressant that inhibits reuptake of serotonin and norepinephrine but, unlike tricyclic antidepressants, has few side effects. The present work studies the antihyperalgesic effect of repeated administrations of VFX (five successive injections of 2.5, 5 or 10 mg/kg, s.c., every half-life) in diabetic rats with the paw pressure test and the effect of the opioid receptor antagonist naloxone (1 mg/kg, i.v.) because an opioidergic mechanism is usually considered to be involved in the analgesic effect of antidepressants. VFX induced a significant dose-dependent increase in vocalization thresholds. This effect was not reversed by naloxone. Thus, we demonstrate a clear antinociceptive effect of VFX which, unlike that of most mixed tricyclic antidepressants, does not involve the endogenous opioid system.
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The effects of maintenance on venlafaxine, which blocks both norepinephrine and serotonin reuptake, on the response to smoked cocaine (0, 12, 25, or 50 mg) in 7 opioid-free and 7 methadone-maintained cocaine abusers was examined during a 42-day study. Participants received venlafaxine (225 mg daily) and placebo as part of a double-blind crossover design. Cocaine significantly increased heart rate, blood pressure, cocaine choice, cocaine ratings, and ratings of positive subjective effects (e.g., "I feel high") in both groups. Venlafaxine significantly decreased the subjective effects of cocaine by 10-20% without affecting cocaine choice or cardiovascular response in both groups. Although the reduction in cocaine's effects was small, further studies using a longer venlafaxine maintenance period or a larger venlafaxine dose are warranted.
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Using in vivo microdialysis in the freely moving rat we have examined the effects of 5-HT(6) receptor antagonism on the neurochemical outcome of antidepressant treatment. Acute administration of both desipramine (10 mg/kg s.c.) and venlafaxine (10 mg/kg s.c.) produced a 2 fold increase in extracellular noradrenaline (NA) but no change in frontal cortex dopamine (DaA), 5-HT or glutamate. Fluoxetine (20 mg/kg s.c.) produced no change in extracellular levels of any of the neurotransmitters examined. SB-271046 produced a 3 fold increase in extracellular glutamate. Combination treatment of SB-271046 with each antidepressant produced no change in the antidepressant-induced changes in NA, DA or 5-HT. In contrast, both fluoxetine and venlafaxine attenuated the SB-271046-induced increase in extracellular glutamate, suggesting that 5-HT and possibly NA may be having an inhibitory action on the excitatory pathways enhanced by 5-HT(6) receptor blockade. Furthermore, these data indicate that the neurochemical effects induced by NA and/or 5-HT reuptake inhibitors are not enhanced by 5-HT(6) receptor blockade indicating that 5-HT(6) receptor antagonists are unlikely to augment the therapeutic efficacy of these types of antidepressants.
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