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Endogenous zinc depresses GABAergic transmission via T-type Ca2+ channels and broadens the time window for integration of glutamatergic inputs in dentate granule cells

A. Grauert,D. Engel,Arnaud Ruiz

Published 2013 in Journal of Physiology

ABSTRACT

•  Zinc inhibits ionotropic receptors commonly found at central synapses, as well as a wide variety of voltage‐activated ion channels that modulate neuronal excitability and neurotransmitter release. •  We found that zinc chelation facilitated GABAergic signalling in dentate granule cells and that blocking T‐type Ca2+ channel activity abolished this effect. Zinc chelation reduced spike threshold, increased spike width and shifted the input–output relationship in dentate interneurones, which is consistent with increased excitability. •  In granule cells, zinc chelation narrowed the window for the integration of glutamatergic inputs originating from perforant path synapses. •  These results demonstrate that zinc modulates dentate interneurone function and regulates spike routing to local and hippocampal targets.

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