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Dual function of Zn2+ on the intrinsic excitability of dopaminergic neurons in rat substantia nigra

Title
Dual function of Zn2+ on the intrinsic excitability of dopaminergic neurons in rat substantia nigra
Authors
Noh J.Chang S.Y.Wang S.Y.Chung J.M.
Ewha Authors
정준모노지현
SCOPUS Author ID
정준모scopus
Issue Date
2011
Journal Title
Neuroscience
ISSN
0306-4522JCR Link
Citation
vol. 175, pp. 85 - 92
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Despite the presence of Zn2+ in high levels in Parkinson brain, it is not yet clearly answered whether and how Zn2+ alters the electrical activity of neurons in substantia nigra (SN). Here we show that Zn2+ alters the intrinsic activity of nigral dopamine neurons in dual ways, that is, excitation or inhibition, by modulating the gating properties of a transient A-type K+ (KA) channel. Depending on the holding potential, Zn2+ could reduce or enhance a transient outward K+ current (IA) in nigral dopamine neurons. Zn2+ slowed the kinetics of both IA activation and inactivation with the rate of activation much more reduced than that of inactivation. Zn2+ also increased the rate of release from IA inactivation. Both activation and inactivation IA curves were shifted by Zn2+ towards positive potentials, but the positive shift of the inactivation curve was much greater than that of the activation curve. We propose that all these effects of Zn2+ on KA channel gating properties underlie the dual mode of Zn2+ action on IA, that is, attenuation or potentiation depending on membrane potential. As a result, Zn2+ increased a bursting activity of a nigral dopamine neuron elicited by anodal break excitation presumably through IA reduction at a hyperpolarizing state, whereas Zn2+ decreased its tonic activity at either resting or depolarizing states where IA was increased. This was further supported by the observations that 4-aminopyridine (4-AP), a well-known KA channel blocker, strengthened or counteracted the effect of Zn2+ on the intrinsic excitability of nigral dopamine neurons. © 2011 IBRO.
DOI
10.1016/j.neuroscience.2010.11.019
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자연과학대학 > 생명과학전공 > Journal papers
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