Abstract:
: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.
journal_name
Nat Neuroscijournal_title
Nature neuroscienceauthors
Hershfinkel M,Kandler K,Knoch ME,Dagan-Rabin M,Aras MA,Abramovitch-Dahan C,Sekler I,Aizenman Edoi
10.1038/nn.2316subject
Has Abstractpub_date
2009-06-01 00:00:00pages
725-7issue
6eissn
1097-6256issn
1546-1726pii
nn.2316journal_volume
12pub_type
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