We found that K+/Cl- co-transporter 2 (KCC2) activity, monitored with wide-field fluorescence, was inhibited by intracellular Zn 2+, a major component of neuronal injury. Zn2+- mediated KCC2 inhibition produced a depolarizing shift of GABA A reversal potentials in rat cortical neurons. Moreover, oxygen-glucose deprivation attenuated KCC2 activity in a Zn2+-dependent manner. The link between Zn2+and KCC2 activity provides a previously unknown target for neuroprotection and may be important in activity-dependent regulation of inhibitory synaptic transmission.
ASJC Scopus subject areas
- Neuroscience (all)