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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Dendritic topology of D1 and D2 medium spiny neurons in the Q-175 mouse model of Huntington's disease

Rubakovic, Anastasia 13 July 2017 (has links)
Direct (D1) and indirect (D2) pathway medium spiny neurons (MSNs) in the striatum are severely affected in Huntington’s disease. The aim of this study was to compare the dendritic topology and electrophysiological properties of wild type (WT) D1 and D2 MSNs with those in the Q-175 mouse model of Huntington’s disease. By scanning biocytin-filled MSNs using high-resolution confocal imaging, we quantified the dendritic lengths and complexity of WT and Q-175+/- D1 and D2 MSNs. We correlated these dendritic topological parameters with various electrophysiological properties. Q175+/- D1 MSNs had significantly larger total dendritic lengths, more complex dendritic arbors, and a larger mean number of primary dendrites than their WT counterparts. Q175+/- D2 MSNs had similar total dendritic lengths, dendritic complexities, and mean number of primary branches as the WT D2 MSNs. WT D1 and D2 MSNs were similar in terms of their total dendritic length, total number of intersections, and mean number of primary dendrites suggesting a degree of homogeneity in these cell populations. We found no correlations between membrane resistance, rheobase, EPSC frequency, or EPSC amplitude, and total dendritic length or dendritic complexity of MSNs when observed separately (WT and Q175+/-) or combined, with one exception, a positive correlation between rheobase and total intersections. These findings add to the understanding of the morphology of D1 and D2 MSNs in general, as well as how they are differentially affected by the presence of a CAG expansion in the Q-175+/- mouse model of Huntington’s disease.

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