Int Rev Neurobiol
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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.
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Despite the progress in understanding the pathophysiology of peripheral nervous system injury and regeneration, as well as advancements in microsurgical techniques, peripheral nerve injuries are still a major challenge for reconstructive surgeons. Thorough knowledge of anatomy, pathophysiology, and surgical reconstruction is a prerequisite of proper peripheral nerve injury management. This chapter reviews the currently available surgical treatment options for different types of nerve injuries in clinical conditions. ⋯ Achieving better outcomes depends both on the advancements in microsurgical techniques and introduction of molecular biology discoveries into clinical practice. The field of peripheral nerve research is dynamically developing and concentrates on more sophisticated approaches tested at the basic science level. Future directions in peripheral nerve reconstruction including, tolerance induction and minimal immunosuppression for nerve allografting, cell based supportive therapies and bioengineering of nerve conduits are also reviewed in this chapter.
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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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Methamphetamine (MAP), a drug of abuse known worldwide for its addictive effects and neurotoxicity, causes somatic and psychiatric disorders. MAP enters terminals/neurons via monoamine transporters, displaces both vesicular and intracellular monoamines, and facilitates the release of monoamines into the extraneuronal space through synaptic transport via the monoamine transporters. Chronic psychostimulant abusers exhibit psychotic features, including delusions and auditory hallucinations. ⋯ The deletion of DAT attenuates the locomotor effects of MAP and may play larger role in behavioral responses to MAP compared to the deletion of VMAT2. MAP produces hyperthermia and/or neuronal toxicity in most species. The effects of MAP in DAT or serotonin transporter (SERT) single knockout (KO) mice and DAT/SERT double KO mice suggested that DAT and SERT are key molecules for hyperthermia and neuronal toxicity of MAP.
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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.