NG2 glial cells distribute extensively in the adult brain and receive direct glutamatergic and GABAergic synaptic innervations from neurons.These cells express Na+ channels,but fail to produce regenerative action potentials.The physiological role of the Na+ channel in these cells is thus unclear.Furthermore,voltage dependent Ca2+ channels,an important Ca2+ entry pathway in many types of cells,can not be detected in these cells.In the present study we found that perfusion of GABA induced Ca2+ elevation in cultured and acute dissociated NG2 cells increased intracellular Ca2+ involving persistent Na+ channels and Na+/Ca2+ exchangers,but not Ca2+ channels,an effect that can be abolished by treatment with sodium channel antagonist TTX,extracellular sodium free solution,calcium free solution,or Na+/Ca2+ exchanger inhibitor KB-R7943,but not by Ca2+ channel inhibitors.Further evidence indicates this unconventional pathway may be also important for Zn2+ uptake known to be crucial for NG2 cell development and injury.