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Introduction. Many known substances affecting the serotoninergic system induce definite physiological effects, including those which are therapeutic. For instance, the enhanced serotoninergic transmission due to decreased functions of autoreceptors and increased inhibitory functions of postsynaptic 5-HT1A is associated with antidepressant effect. The central serotoninergic system takes part in the regulation of many bodily functions, such as sleep, wakefulness, blood pressure, pain perception or sexual behaviours. Moreover, it is involved in the pathogenesis of depression, anxiety, addictions, migraine and other headaches. In pain therapy, not only typical analgesics are used, but also substances without obvious analgesic effect, thus allowing potential pharmacological modulation of analgesic activity in the treatment of pain. Objective. The aim of the study was to determine whether a chemical lesion to the central noradrenergic system at an early stage of individual development alters reactivity of 5-HT3 receptors in adult rats. Materials and method. The study used newborn and adult Wistar rats aged 8–10 weeks. Behavioural tests (writhing test, formalin assay) were used to assess the analgesic action of ondansetron as a 5-HT3 receptor antagonist. Results. The analgesic effect of ondansetron (1.0 mg/kg b.w., i.p.) in the writhing test was weak and short. Pain intensity score after ondansetron injection (1.0 mg/kg b.w., i.p) was 2–3 points and did not differ significantly between the study groups. Conclusions. Damage to the central noradrenergic system at an early stage of individual development has no effect on the antinociceptive effects of the serotonin (5-HT3) receptor antagonist, ondansetron, in the persistent pain model.
The electromagnetic fields (EMFs) have been shown to alter animal and human behavior, such as directional orientation, learning, pain perception (nociception or analgesia) and anxiety-related behaviors. The aim of this study was to evaluate the influence of electromagnetic fields of high-frequency microwaves on pain perception and anti-nociceptive activity of tramadol (TRAM) - analgetic effective in the treatment of moderate to severe acute and chronic pain states. Electromagnetic fields exposures of a) 1500 MHz frequency and b) modulated, 1800 MHz (which is identical to that generated by mobile phones) were applied. Paw withdrawal latency (PWL) to thermal stimulus was measured in vehicle or tramadol (TRAM) treated animals before and after 30, 60 and 90 minutes from injections. The differences in the level of pain (PWL) between control group and rats exposed to EMF alone in three measurements, were not observed. Tramadol alone significantly increased PWLs to thermal stimulus in comparison to vehicle results at 30 (p < 0.001) and 60 minutes (p < 0.05) after drug injection. EMF exposure of both frequencies transiently suppressed analgesic effect of tramadol, significantly reducing paw withdrawal latency in animals treated with this drug at 30 minutes from the drug injection.
Opioids administered by intracerebroventricular injections produce analgesic responses in rats. The present study was undertaken to investigate the effects of a highly selective m-opioid receptor ligand morphiceptin on trigemino-hypoglossal reflex in rats. The analgesic effect of morphiceptin was compared with another opioid peptide, Met-enkephalin. With the experimental settings used in this study, we have demonstrated that both morphiceptin and Met-enkephalin show significant dose-dependent analgesic effects after i.c.v. administration in rats as assayed by trigemino-hypoglossal reflex test. The antinociceptive response to Met-enkephalin was short lasting and was observed 10 to 15 min after i.c.v. perfusion. Morphiceptin had a relatively longer duration of antinociceptive action, the effect was observed 20- 50 min after i.c.v. perfusion. Neither morphiceptin nor Met-enkephalin produced antinociception after peripheral injections. The results of the present study indicate that both tested peptides act at µ-opioid receptors situated in the central nervous system. They also suggest that µ-opioid receptors present in the central nervous system are an important element of the trigemino-hypoglossal reflex arc. For that reason selective m-opioid receptor ligands, like morphiceptin, inhibit the reflex more significantly.
Development of neuropathic pain is accompanied by many changes in immune and glial cells. These changes correspond to activation of immune and glial cells that have been shown to influence the opioid effectiveness and can be modulated by minocycline (a potent inhibitor of microglial activation). In earlier study we have demonstrated that function of opioidergic neurons may be modulated by the immune system. These changes have been shown to be responsible for the efficacy of opioids. The aim of our study was to examine the effect of the minocycline-triggered inhibition of microglia activation on the injury-induced changes and the efficacy of mu and delta opioid receptor ligands in a rat model of neuropathic pain (chronic constriction injury to the sciatic nerve). In cell culture studies, we examined the influence of opioids (morphine, DAMGO, DPDPE, deltorphin II) on activated primary cultured rat microglia by using MTT and/or NO assays. All experiments were performed according to the IASP recommendations and were approved by a local Bioethics Committee. On the spinal cord level the injury to the sciatic nerve induced an up-regulation of IL-1beta, IL-6 expression, CX3CR1 and C1q (marker of microglia, macrophage and leukocyte activation). Chronic administration of minocycline not only diminished neuropathic pain-related behavior and C1q-positive cell activation, but also attenuate the changes in proinflammatory factors like IL1beta, IL-6 and CX3CR1 in the spinal cord and DRG. In in vivo experiments, the analgesic effects of mu-opioid (morphine and DAMGO), but not delta-opioid (DPDPE, deltorphin II) receptor ligands were lower in the rats under neuropathic pain. Moreover, the analgesic effects of morphine and DAMGO, but not DPDPE and deltorphin II were significantly potentiated by minocycline chronic administration. Our in vitro findings that non-stimulated microglia cells respond differently to opioids in comparisons with stimulated cells as measured by MTT and/or NO assays, corresponded well with the results of in vivo studies. Our study underlined that inhibition of microglial activation could differently influence analgesic effects of mu- but not delta-opioid ligands in injury-induced pathologies, which may influence the effect of various opioid drugs used in chronic pain therapy.
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