Pharmacol Rep
-
The treatment of neuropathic pain resulting from nervous system malfunction remains a challenging problem for doctors and scientists. The lower effectiveness of conventionally used analgesics in neuropathic pain is associated with complex and not fully understood mechanisms of its development. Undoubtedly, interactions between immune and nervous system are crucial for maintenance of painful neuropathy. ⋯ This review discusses the role of chemokines from all four subfamilies as essential mediators of neuron-glia interactions occurring under neuropathic pain conditions. Based on available data, we analyse the influence of chemokines on opioid properties. Finally, we identify new direct and indirect pharmacological targets whose modulation may result in effective therapy of neuropathic pain, possibly in combination with opioids.
-
Tapentadol is a centrally acting analgesic with a dual mode of action as a μ-opioid receptor (MOR) agonist and a noradrenaline reuptake inhibitor (NRI). It was initially approved by the US Food and Drug Administration in November 2008 for the treatment of moderate-to-severe acute pain in adult patients, and in August 2011, for chronic pain in an prolonged release form in the same population. ⋯ It appears to be well-tolerated and effective in the treatment of moderate-to severe acute and chronic pain. Owing to its dual mechanism of action, it is hypothesized to be good option in the treatment of both nociceptive and neuropathic pain.
-
The aim of this study was to investigate this involvement in not inflammatory model of pain and which opioid receptor subtype mediates noradrenaline-induced peripheral antinociception. Noradrenaline is involved in the intrinsic control of pain-inducing pro-nociceptive effects in the primary afferent nociceptors. However, inflammation can induce various plastic changes in the central and peripheral noradrenergic system that, upon interaction with the immune system, may contribute, in part, to peripheral antinociception. ⋯ Besides the α2-adrenoceptor, the present data provide evidence that, in absence of inflammation, NA activating α1 and β-adrenoceptor induce endogenous opioid release to produce peripheral antinociceptive effect by μ and δ opioid receptors.