Loss of glycinergic and GABAergic inhibition in chronic pain--contributions of inflammation and microglia.
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.
Zeilhofer
Hanns Ulrich
HU
Institute of Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland. Zeilhofer@pharma.uzh.ch <Zeilhofer@pharma.uzh.ch>
D000818:Animals; D002908:Chronic Disease; D015232:Dinoprostone / Q000502:physiology; D005998:Glycine / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000150:complications*; D017628:Microglia / Q000502:physiology*; D009433:Neural Inhibition; D010146:Pain / Q000209:etiology* / Q000503:physiopathology; D013569:Synapses / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D005680:gamma-Aminobutyric Acid; D015232:Dinoprostone; D005998:Glycine