Antidepressants for neuropathic pain: A Cochrane review
- SourceAvailable from: Engin Ciftcioglu
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- "Together, these results suggest that α 2A -/α 2C -adrenoceptors and 5-HT 2 /5-HT 4 receptor-modulated mechanisms may be responsible for the antinociceptive effect of imipramine on visceral pain in rats. Despite the proven antinociceptive effects of antidepressants revealed by experimental studies in animals (Fishbain et al., 2000; Micó et al., 2006) and the clinical studies that recommend the use of antidepressants for the management of certain pain states (Onghena and Van Houdenhove, 1992; O'Malley et al., 2000; Saarto and Wiffen, 2010), the exact mechanism(s) of the analgesic actions of antidepressants remain unknown and require elucidation. The major mechanism of antidepressant-mediated antinociception has been suggested to be the blockade of the reuptake of monoamines via the inhibition of their specific transporters at the presynaptic membrane (Millan, 2002; Micó et al., 2006). "
ABSTRACT: It has been shown that imipramine, a tricyclic antidepressant (TCA), is a potent analgesic agent. However, the effect of imipramine on visceral pain has not been extensively investigated. In the current study, our aim was to characterize the putative analgesic effect of intravenous imipramine on visceral pain in rats. Our second aim was to assess the involvement of serotonergic (5-HT2, 3, 4) and noradrenergic (α2A, 2B, 2C) receptor subtypes in this putative antinociceptive effect of imipramine. Male Sprague Dawley rats (250-300 g) were implanted with venous catheters for drug administration and implanted with enamelled nichrome electrodes for electromyography of the external oblique muscles. Noxious visceral stimulation was applied via by colorectal distension (CRD). The visceromotor responses (VMRs) to CRD were quantified electromyographically before and after imipramine administration at 5, 15, 30, 60, 90 and 120 min. In the antagonist groups, the agents were administered 10 min before imipramine. The administration of imipramine (5-40 mg/kg) produced a dose-dependent reduction in VMR. The administration of yohimbine (a nonselective α2-adrenoceptor antagonist, 1 mg/kg), BRL-44408 (an α2A-adrenoceptor antagonist, 1 mg/kg) or MK-912 (an α2C-adrenoceptor antagonist, 300 μg/kg) but not imiloxan (an α2B-adrenoceptor antagonist, 1 mg/kg) inhibited the antinociceptive effect of imipramine (20 mg/kg). Additionally, ketanserin (a 5-HT2 receptor antagonist, 0.5, 1, and 2 mg/kg) and GR113808 (a 5-HT4 receptor antagonist, 1 mg/kg) enhanced and ondansetron (a 5-HT3 receptor antagonist, 0.5, 1, and 2 mg/kg) failed to alter the imipramine-induced antinociceptive effect. Our data demonstrated that, in the CDR-induced rat visceral pain model, intravenous imipramine appeared to have antinociceptive potential and that α2A-/α2C-adrenoceptors and 5-HT2/5-HT4 receptors may be responsible for the antinociceptive effect of imipramine on visceral pain in rats.Pharmacology Biochemistry and Behavior 07/2014; DOI:10.1016/j.pbb.2014.02.017 · 2.82 Impact Factor
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- "Several systematic reviews indicate that TCAs are effective in neuropathic pain and PHN (Attal et al., 2010; Hempenstall et al., 2005; Niv & Maltsman-Tseikhin, 2005), being superior to Selective Serotonin Reuptake Inhibitors (SSRI) (Attal et al., 2006; Saarto & Wiffen, 2010). No studies assessed the use of Serotonin-Noradrenalin Reuptake Inhibitors (SNRI) for this condition. "
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- "Antidepressants have a genuine analgesic action that has been demonstrated in both experimental and clinical conditions (Fishbain et al., 2000; Micó et al., 2006). Furthermore, a wealth of clinical literature advocates the use of antidepressants in the management of certain pain states with or without co-existing depression (O'Malley et al., 2000; Onghena and Van Houdenhove, 1992; Saarto and Wiffen, 2010). However, compared to other analgesic drugs, antidepressants are perhaps the least well-known in terms of analgesic mechanism of action. "
ABSTRACT: Tianeptine is an unusual tricyclic antidepressant drug. In this study, we aimed to investigate the antinociceptive effect of tianeptine on visceral pain in rats and to determine whether possible antinociceptive effect of tianeptine is mediated by serotonergic (5-HT(2,3)) and noradrenergic (α(1,2)) receptor subtypes. Male Sprague Dawley rats (250-300 g) were supplied with a venous catheter, for drug administrations, and enameled nichrome electrodes, for electromyography, at external oblique musculature. Colorectal distension (CRD) was employed as the noxious visceral stimulus and the visceromotor response (VMR) to CRD was quantified electromyographically before and 5, 15, 30, 60, 90 and 120 min after tianeptine administration. Antagonists were administered 10 min before tianeptine for their ability to change tianeptine antinociception. Intravenous administration of tianeptine (2.5-20 mg/kg) produced a dose-dependent reduction in VMR. Administration of 5-HT(3) receptor antagonist ondansetron (0.5, 1 and 2 mg/kg), but not 5-HT(2) receptor antagonist ketanserine (0.5, 1 and 2 mg/kg), reduced the antinociceptive effect of tianeptine (10mg/kg). In addition, administration of α(1)-adrenoceptor antagonist prazosin (1 mg/kg) or α(2)-adrenoceptor antagonist yohimbine (1 mg/kg) did not cause any significant effect on the tianeptine-induced antinociception. Our data indicate that intravenous tianeptine exerts a pronounced antinociception against CRD-induced visceral pain in rats, and suggests that the antinociceptive effect of tianeptine appears to be mediated in part by 5-HT(3) receptors, but does not involve 5-HT(2) receptors or α-adrenoceptors.European journal of pharmacology 02/2012; 681(1-3):44-9. DOI:10.1016/j.ejphar.2012.01.043 · 2.68 Impact Factor