Silencing the α2 Subunit of γ-aminobutyric Acid Type A Receptors in Rat Dorsal Root Ganglia Reveals Its Major Role in Antinociception Posttraumatic Nerve Injury

Background Neuropathic pain is likely the result of repetitive high frequency bursts of peripheral afferent activity leading to long-lasting changes in synaptic plasticity in the spinal dorsal horn (DH). Drugs that promote GABA activity in the DH provide partial relief of neuropathic symptoms. We examined how in vivo silencing of the GABAA α2 gene in DRG controls of NPP.