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      Involvement of microglia in the ethanol-induced neuropathic pain-like state in the rat.

      Neuroscience Letters
      Afferent Pathways, drug effects, pathology, physiopathology, Alcoholic Neuropathy, metabolism, Animals, Biological Markers, analysis, Calcium-Binding Proteins, Central Nervous System Depressants, adverse effects, Ethanol, Hyperalgesia, chemically induced, Hypertrophy, Male, Microfilament Proteins, Microglia, Neurons, Afferent, Pain Measurement, Pain Threshold, physiology, Peripheral Nerves, Rats, Rats, Inbred F344, Spinal Cord, Up-Regulation

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          Abstract

          Central mechanisms of neuropathy induced by chronic ethanol treatment are almost unknown. In this study, rats were treated with ethanol-diet for 72 days. Mechanical hyperalgesia was observed during ethanol consumption, even after ethanol withdrawal. Under these conditions, a microglial marker ionized calcium-binding adaptor molecule 1-, but not a neuron marker microtuble associated protein-2-, like immunoreactivies were increased in the rat spinal cord. Furthermore, hypertrophy of microglia was clearly observed following chronic ethanol consumption. These findings support the idea that the activation and hypertrophy of microglia in the spinal cord may be, at least in part, associated with in the induction of ethanol-dependent neuropathic pain-like state.

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