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Permanent URI for this collectionhttps://hdl.handle.net/20.500.14288/3

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Department: search.filters.department.Department of Chemical and Biological EngineeringSubject: search.filters.subject.Multidisciplinary sciences

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    Impaired inhibitory GABAergic synaptic transmission and transcription studied in single neurons by Patch-seq in Huntington's disease
    (National Academy of Sciences, 2021) Paraskevopoulou, Foteini; Parvizi, Poorya; Senger, Gokce; Rosenmund, Christian; Yildirim, Ferah; Department of Chemical and Biological Engineering; Department of Chemical and Biological Engineering; Tunçbağ, Nurcan; Faculty Member; College of Engineering; 245513
    Transcriptional dysregulation in Huntington's disease (HD) causes functional deficit s in striatal neurons. Here, we performed Patch-sequencing (Patch-seq) in an in vitro HD model to investigate the effects of mutant Huntingtin (Htt ) on synaptic transmission and gene transcription in single striatal neurons. We found that expression of mutant Htt decreased the synaptic output of striatal neurons in a cell autonomous fashion and identified a number of genes whose dysregulation was correlated with physiological deficiencies in mutant Htt neurons. In support of a pivotal role for epigenetic mechanisms in HD pathophysiology, we found that inhibiting histone deacetylase 1/3 activities rectified several functional and morphological deficit s and alleviated the aberrant transcriptional profiles in mutant Htt neurons. With this study, we demonstrate that Patch-seq technology can be applied both to better understand molecular mechanisms underlying a complex neurological disease at the single-cell level and to provide a platform for screening for therapeutics for the disease.