HCN channelopathy in external globus pallidus neurons in models of Parkinson s disease

S. Chan, K. Glajch, T. Gertler, J. Guzmán, J. Mercer, A. Lewis, A. Goldberg, T. Tkatch, R. Shigemoto, S. Fleming, D. Chetkovich, P. Osten, H. Kita, J. Surmeier, Nature Neuroscience 14 (2011) 85–94.

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Author
Chan, Savio; Glajch, Kelly E; Gertler, Tracy S; Guzmán, Jaime N; Mercer, Jeff N; Lewis, Alan S; Goldberg, Alan B; Tkatch, Tatiana; Shigemoto, RyuichiIST Austria ; Fleming, Sheila M; Chetkovich, Dane M; Osten, Pavel
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Abstract
Parkinson's disease is a common neurodegenerative disorder characterized by a profound motor disability that is traceable to the emergence of synchronous, rhythmic spiking in neurons of the external segment of the globus pallidus (GPe). The origins of this pathophysiology are poorly defined for the generation of pacemaking. After the induction of a parkinsonian state in mice, there was a progressive decline in autonomous GPe pacemaking, which normally serves to desynchronize activity. The loss was attributable to the downregulation of an ion channel that is essential in pacemaking, the hyperpolarization and cyclic nucleotide-gated (HCN) channel. Viral delivery of HCN2 subunits restored pacemaking and reduced burst spiking in GPe neurons. However, the motor disability induced by dopamine (DA) depletion was not reversed, suggesting that the loss of pacemaking was a consequence, rather than a cause, of key network pathophysiology, a conclusion that is consistent with the ability of L-type channel antagonists to attenuate silencing after DA depletion.
Publishing Year
Date Published
2011-01-01
Journal Title
Nature Neuroscience
Volume
14
Issue
1
Page
85 - 94
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Chan S, Glajch K, Gertler T, et al. HCN channelopathy in external globus pallidus neurons in models of Parkinson s disease. Nature Neuroscience. 2011;14(1):85-94. doi:10.1038/nn.2692
Chan, S., Glajch, K., Gertler, T., Guzmán, J., Mercer, J., Lewis, A., … Surmeier, J. (2011). HCN channelopathy in external globus pallidus neurons in models of Parkinson s disease. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.2692
Chan, Savio, Kelly Glajch, Tracy Gertler, Jaime Guzmán, Jeff Mercer, Alan Lewis, Alan Goldberg, et al. “HCN Channelopathy in External Globus Pallidus Neurons in Models of Parkinson s Disease.” Nature Neuroscience. Nature Publishing Group, 2011. https://doi.org/10.1038/nn.2692.
S. Chan et al., “HCN channelopathy in external globus pallidus neurons in models of Parkinson s disease,” Nature Neuroscience, vol. 14, no. 1. Nature Publishing Group, pp. 85–94, 2011.
Chan S, Glajch K, Gertler T, Guzmán J, Mercer J, Lewis A, Goldberg A, Tkatch T, Shigemoto R, Fleming S, Chetkovich D, Osten P, Kita H, Surmeier J. 2011. HCN channelopathy in external globus pallidus neurons in models of Parkinson s disease. Nature Neuroscience. 14(1), 85–94.
Chan, Savio, et al. “HCN Channelopathy in External Globus Pallidus Neurons in Models of Parkinson s Disease.” Nature Neuroscience, vol. 14, no. 1, Nature Publishing Group, 2011, pp. 85–94, doi:10.1038/nn.2692.

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