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KMID : 0355820200410010065
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Korean Journal of Oral Anatomy
2020 Volume.41 No. 1 p.65 ~ p.74
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Disinhibition in pathological pain
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Bae Yong-Chul
Ko Hyoung-Gon
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Abstract
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Noxious and tactile stimuli are transmitted into the spinal cord or in the trigeminal nucleus before being delivered to the brain. Inhibitory interneurons are distributed throughout these relay regions and modulate sensory stimuli by inhibiting primary afferent terminals (presynaptic inhibition) and spinal interneurons (postsynaptic inhibition) by releasing γ-aminobutyric acid (GABA) and/or glycine. Regarding pathological pain, the spinal inhibitory interneurons are involved in hyperalgesia, allodynia, spontaneous pain, and referred pain. Disinhibition is the loss of inhibitory power mediated by the inhibitory interneurons, underlying these symptoms. Studies on global GABAergic neurons have shown that dysregulation of intracellular Cl? concentration, death of inhibitory interneurons, and change of electrophysiological properties are the mechanisms underlying disinhibition. Recent studies exploring the connectivity and function of each specific class of inhibitory interneurons using neurochemical markers will strengthen the basic knowledge of disinhibition in inhibitory interneuron and help develop novel and effective treatments for pathological pain.
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KEYWORD
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disinhibition, pathological pain, inhibitory interneuron
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