Vector-mediated release of GABA attenuates pain-related behaviors and reduces Na(V)1.7 in DRG neurons.

ABSTRACT: Pain is a common and debilitating accompaniment of neuropathy that occurs as a complication of diabetes. In the current study, we examined the effect of continuous release of gamma amino butyric acid (GABA), achieved by gene transfer of glutamic acid decarboxylase (GAD67) to dorsal root ganglia (DRG) in vivo using a non-replicating herpes simplex virus (HSV)-based vector (vG) in a rat model of painful diabetic neuropathy (PDN). Subcutaneous inoculation of vG reduced mechanical hyperalgesia, thermal hyperalgesia and cold allodynia in rats with PDN. Continuous release of GABA from vector transduced cells in vivo prevented the increase in the voltage-gated sodium channel isoform 1.7 (Na(V)1.7) protein that is characteristic of PDN. In vitro, infection of primary DRG neurons with vG prevented

SUBMITTER: Chattopadhyay M 

PROVIDER: S-EPMC3321314 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature