This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License 4.0 (CC BY-NC-ND 4.0), which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
Altered neuronal activity in the striatum appears to be a key component of Huntington’s disease (HD), a fatal, neurodegenerative condition. To assess this hypothesis in freely behaving transgenic rats that model HD (tgHDs), we used chronically implanted micro-wires to record the spontaneous activity of striatal neurons. We found that relative to wild-type controls, HD rats suffer from population-level deficits in striatal activity characterized by a loss of correlated firing and fewer episodes of coincident spike bursting between simultaneously recorded neuronal pairs. These results are in line with our previous report of marked alterations in the pattern of striatal firing in mouse models of HD that vary in background strain, genetic construct, and symptom severity. Thus, loss of coordinated spike activity in striatum appears to be a common feature of HD pathophysiology, regardless of HD model variability.
Miller, B. R., Walker, A. G., Fowler, S. C., von Hörsten, S., Riess, O., Johnson, M. A., & Rebec, G. V. (2010). Dysregulation of coordinated neuronal firing patterns in striatum of freely behaving transgenic rats that model Huntington’s disease. Neurobiology of Disease, 37(1), 106–113. http://doi.org/10.1016/j.nbd.2009.09.013
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