Dorsal Horn Parvalbumin Neurons Are Gate-Keepers of Touch-Evoked Pain after Nerve Injury
Disinhibition
Allodynia
Nerve Injury
Interneuron
DOI:
10.1016/j.celrep.2015.09.080
Publication Date:
2015-11-03T08:00:58Z
AUTHORS (13)
ABSTRACT
Neuropathic pain is a chronic debilitating disease that results from nerve damage, persists long after the injury has subsided, and characterized by spontaneous mechanical hypersensitivity. Although loss of inhibitory tone in dorsal horn spinal cord major contributor to neuropathic pain, molecular cellular mechanisms underlying this disinhibition are unclear. Here, we combined pharmacogenetic activation selective ablation approaches mice define contribution parvalbumin (PV)-expressing interneurons naive conditions. Ablating PV neurons produce pain-like allodynia via PKCγ excitatory interneurons. Conversely, activating nerve-injured alleviates These findings indicate modality-specific filters gate but not thermal inputs increasing interneuron activity can ameliorate hypersensitivity develops following injury.
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