Journal
NATURE NEUROSCIENCE
Volume 12, Issue 6, Pages 725-727Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2316
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Funding
- US-Israel Binational Science Foundation [BSF2007121]
- US National Institutes of Health [NS043277, DC004199]
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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. Zn(2+) 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 Zn(2+)-dependent manner. The link between Zn(2+) and KCC2 activity provides a previously unknown target for neuroprotection and may be important in activity-dependent regulation of inhibitory synaptic transmission.
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