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Tramadol, which inhibits the reuptake of noradrenaline and serotonin, is effective in animal models of depression. Its antidepressant-like effects may be mediated mainly by the noradrenergic system. This study investigated the role of the noradrenergic system in the antidepressant-like effects of tramadol and desipramine in the unpredictable chronic mild stress model. We assessed the involvement of beta-adrenoreceptors, particularly beta2-receptors in the activity of these drugs. In addition, we measured the level of noradrenaline and its metabolite 3-methoxy-4-hydroxy-phenylglycol (MHPG) in the locus coeruleus, hypothalamus, hippocampus and cerebellum in stressed mice. Unpredictable chronic mild stress induced a degradation of coat state and decreased grooming behaviour in the splash test, which was reversed by the chronic administration of tramadol (20 mg/kg) and desipramine (10 mg/kg). The nonselective beta-adrenoreceptor antagonist propranolol (5 mg/kg, intraperitoneally) and the selective beta2-receptor antagonist ICI 118,551 (2 mg/kg, intraperitoneally) reversed the antidepressant-like effects of tramadol and desipramine. Moreover, chronic tramadol and desipramine treatment increased the level of noradrenaline (NA) and MHPG in the locus coeruleus but not in the cerebellum, whereas only MHPG level was increased in the hypothalamus. Tramadol, however, increased the levels of MHPG and NA in the hippocampus, whereas desipramine only increased NA level. These data support the view that the noradrenergic system plays an important role in the antidepressant-like action of tramadol.

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Plants provide a wealth of bioactive compounds which aid in exerting a substantial strategy for the treatment of neurological disorders such as Alzheimer's disease and dementia.

The antinociceptive effect of dipyrone, a nonsteroidal anti-inflammatory drug, was studied in a series of experiments employing tail-flick and hot-plate models and the abdominal constrictor test. The drug was given via intracerebroventricular (ICV), intrathecal (IT) or subcutaneous (SC) routes. Dipyrone exhibited no analgesic activity in the tail-flick and hotplate tests while it inhibited the number of stretches in a dose-dependent manner. The antinociceptive effect of dipyrone administered by the ICV and IT routes was almost completely reversed by naloxone treatment. The same procedure attenuated but not completely inhibited the dipyrone action induced by SC administration. Histopathological examination revealed that IT dipyrone application produces no significant lesion in the spinal cord. The results suggest that dipyrone may exert a central antinociceptive action reversed by naloxone.

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