Loss of glycinergic and GABAergic inhibition in chronic pain--contributions of inflammation and microglia

International Immunopharmacology
Hanns U Zeilhofer

Abstract

Tissue trauma, inflammation and neuropathy can under unfortunate condition progress into chronic pain syndromes. It is meanwhile generally accepted that chronic pain, i.e. pain, which persists beyond the resolution of tissue traumata and inflammation, is due to plastic changes in the neuronal processing of sensory stimuli in the CNS. A loss of synaptic inhibition (i.e. dis-inhibition) in the spinal cord dorsal horn has been increasingly recognized as an important process in the development and maintenance of chronic pain of both inflammatory and neuropathic origin. Although inflammation and neuropathy involve distinct mechanisms of synaptic dis-inhibition, the production of inflammatory mediators and/or the activation of immune cells, two events that have once been thought to be normally excluded from the CNS, appear to be critical for both conditions.

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Citations

Mar 5, 2009·Journal of Molecular Medicine : Official Organ of the Gesellschaft Deutscher Naturforscher Und Ärzte·Hanns Ulrich ZeilhoferKatharina Hösl
Dec 17, 2009·Acta Neuropathologica·Manuel B Graeber, Wolfgang J Streit
Jan 20, 2011·The Journal of Biological Chemistry·Esperanza JiménezBeatriz López-Corcuera
Jun 3, 2011·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Robert WitschiHanns Ulrich Zeilhofer
Aug 18, 2010·International Journal of Medical Sciences·Fei-xiang WuWei-feng Yu
Sep 18, 2012·Neurochemical Research·Salvador Quiróz-GonzálezIsmael Jiménez-Estrada
Feb 9, 2012·European Journal of Pharmacology·Jun-Xu Li, Yanan Zhang
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Nov 3, 2010·Neuropharmacology·Hanns Möhler
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