Neuropharmacology
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Ischemia is a multifactorial pathology characterized by different events evolving in the time. After ischemia a primary damage due to the early massive increase of extracellular glutamate is followed by activation of resident immune cells, i.e microglia, and production or activation of inflammation mediators. Protracted neuroinflammation is now recognized as the predominant mechanism of secondary brain injury progression. ⋯ Among P2Y receptors, antagonists of P2Y12 receptors are of value because of their antiplatelet activity and possibly because of additional anti-inflammatory effects. Moreover strategies that modify adenosine or ATP concentrations at injury sites might be of value to limit damage after ischemia. This article is part of the Special Issue entitled 'Purines in Neurodegeneration and Neuroregeneration'.
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Neuropathic pain, a chronic pain condition following nerve damage and degeneration, involves aberrant excitability in the dorsal horn of the spinal cord. A growing body of evidence has shown that the aberrant excitability might not be a consequence merely of changes in neurons, but rather of multiple alterations in glial cells, such as microglia, the immune cells of the central nervous system. ⋯ Here, we describe recent advances in the understanding of neuron-microglia interactions by purinergic signaling in neuropathic pain following neurodegeneration. This article is part of the Special Issue entitled 'Purines in Neurodegeneration and Neuroregeneration'.