Int Rev Neurobiol
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Review Historical Article
Chapter 1: Peripheral nerve repair and regeneration research: a historical note.
Although the most significant advances in nerve repair and regeneration have been acquired over the last few decades, the study of nerve repair and regeneration potential dates back to ancient times namely to Galen in the second century A. D. ⋯ In particular, we focus on the nineteenth century and the first decades of the twentieth century, an age in which the fathers of neurosurgery and neurobiology established the basis for most of the nerve repair and regeneration concepts used today. Finally, we shine a light on the most current history to show how recent pressure to use modern interdisciplinary and translational approach represents a sort of rediscovery of the scientific habits of the fathers of modern biomedicine, who used to carry out research from an integrated and broad point of view rather than from a super-specialized and specific one as it is often used today.
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Neuropathic pain is one of the worst painful symptoms in clinic. It contains nerve-injured neuropathy, diabetic neuropathy, chronic inflammatory pain, cancer pain, and postherpes pain, and is characterized by a tactile allodynia and hyperalgesia. Neuropathic pain, especially the nerve-injured neuropathy, the diabetic neuropathy, and the cancer pain, is opioid resistant pain. ⋯ These drugs show remarkable effectiveness against hyperalgesia and allodynia during neuropathic pain states. Oxycodone is a mu-opioid receptor agonist, which has different pharmacological profiles with morphine. The remarkable effectiveness of oxycodone for neuropathic pain provides the possibility that mu-opioid receptor agonists, which have different pharmacological profile with morphine, can be used for the management of neuropathic pain.
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Elucidation of the mechanism of neuropathic pain caused by vincristine is required because long-term treatment with this anticancer agent often causes neuropathic pain. We refer to the involvement of inflammatory mediators in vincristine-induced neuropathic pain in this review. Several reports using rodents have shown that long-lasting neuropathic pain (mechanical allodynia) is caused by repeated systemic injection of vincristine. ⋯ In the CNS, these inflammatory cytokines have an important role in the neuropathic pain caused by vincristine. Immune-modulating agents that prevent activation of immune cells and/or the inhibitory agents of inflammatory cytokines could prevent the neuropathic pain caused by vincristine. These agents could increase the tolerability of vincristine when used for the treatment of leukemia and lymphoma.
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Morphine-3-glucuronide (M3G), a main metabolite of morphine, has been proposed as a responsible factor when patients present with the neuroexcitatory side effects (allodynia, hyperalgesia, and myoclonus) observed following systemic administration of large doses of morphine. Indeed, both high-dose morphine (60 nmol/5 microl) and M3G (3 nmol/5 microl) elicit allodynia when administered intrathecally (i.t.) into mice. The allodynic behaviors are not opioid receptor mediated. ⋯ Furthermore, the increased release of NO observed after i.t. injection of M3G activates astrocytes and induces the release of the proinflammatory cytokine, interleukin-1beta. Taken together, these findings suggest that M3G may induce allodynia via activation of NO-ERK pathway, while maintenance of the allodynic response may be triggered by NO-activated astrocytes in the dorsal spinal cord. The demonstration of the cellular mechanisms of neuronal-glial interaction underlying M3G-induced allodynia provides a fruitful strategy for improved pain management with high doses of morphine.
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During the last years, we have focused on the study of the neurotoxic effects of 3,4-methylenedioxymethamphetamine (MDMA) and methamphetamine (METH) on the central nervous system (CNS) and their pharmacological prevention methods. In the process of this research, we have used a semipurified synaptosomal preparation from striatum of mice or rats as a reliable in vitro model to study reactive oxygen species (ROS) production by these amphetamine derivatives, which is well-correlated with their dopaminergic injury in in vivo models. Using this preparation, we have demonstrated that blockade of alpha7 nicotinic receptors with methyllycaconitine (MLA) prevents ROS production induced by MDMA and METH. ⋯ In all the cases, MDMA displayed higher affinity than METH and it was higher for heteromeric than for alpha7 subtype. Pre-incubation of differentiated PC12 cells with MDMA or METH induces nAChR upregulation in a concentration- and time-dependent manner, as many nicotinic ligands do, supporting their functional interaction with nAChRs. Such interaction expands the pharmacological profile of amphetamines and can account for some of their effects.