Objective: 

Gamma-aminobutyric acid (GABA) signaling components are not only highly expressed throughout the central nervous system (CNS), but also widely distributed in many non-neuronal tissues. Our objective is to investigate the expression and function of GABA-A channels in pancreatic islets (human) and T cells (human, rat and mouse). Methods. Quantitative PCR analysis, Western blot, immunohistochemistry, patch-clamp and hormone release experiments were performed. Results. Multiple GABA-A channel subunits were detected in human islets. The expression of a1, a2, b2 and b3 GABA-A channel subunits were down-regulated in islets from type 2 diabetic individuals. Endogenous GABA produced within the islets evoked tonic currents in the cells. The currents were enhanced by pentobarbital and inhibited by the GABA-A antagonist, SR95531. The effects of SR95531 on hormone release revealed that activation of GABA-A channels decreased both insulin and glucagon secretion. The profile of GABA-A channel subunits detected in T cells differs between the species and GABA-evoked currents were recorded in T cells.

Conclusions: 

Interstitial GABA effectively activates GABA-A channels in pancreatic a and b cells. The inter-species difference of GABA-A channel subtypes in T cells may result in distinct responses to GABAergic drugs.