We show that (1) Cav3.2 channels are specifically expressed in GABAergic parvalbumin (PV)-expressing neurons of the APT; (2) bursting activity of these neurons is increased in the SNI model of neuropathic pain; (3) the Cav3.2 channel contribution to the bursting activity of the PV-expressing neurons is enhanced in the SNI model, and (4) their specific deletion in the APT significantly reduces both the initiation and maintenance of neuropathic mechanical and cold allodynia in the SNI model. The gene discussed is CACNA1H; the disease is neuropathic pain.