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Until recently, it was believed that striatal interneurons were spared from degeneration. This view has changed after the demonstration that parvalbumin (\n                    <jats:styled-content style=\"fixed-case\">PV<\/jats:styled-content>\n                    )\u2010expressing interneurons also are vulnerable in humans. Here we compared morphological and functional changes of striatal fast\u2010spiking interneurons (\n                    <jats:styled-content style=\"fixed-case\">FSI<\/jats:styled-content>\n                    s) and low\u2010threshold spiking (\n                    <jats:styled-content style=\"fixed-case\">LTS<\/jats:styled-content>\n                    ) interneurons in the Q175 mouse model of\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    at presymptomatic (2\u00a0months) and symptomatic (12\u00a0months) stages of the disease. Electrophysiological intrinsic and synaptic properties of\n                    <jats:styled-content style=\"fixed-case\">FSI<\/jats:styled-content>\n                    s were significantly altered in symptomatic mice compared to wild\u2010type (\n                    <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>\n                    ) littermates. Overall,\n                    <jats:styled-content style=\"fixed-case\">FSI<\/jats:styled-content>\n                    s became more excitable with disease progression. Sholl analysis also revealed a significant loss of dendritic complexity and excitatory synaptic inputs. The basic membrane and synaptic properties of\n                    <jats:styled-content style=\"fixed-case\">LTS<\/jats:styled-content>\n                    interneurons were similar in Q175 and\n                    <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>\n                    mice regardless of disease stage. The resilience of\n                    <jats:styled-content style=\"fixed-case\">LTS<\/jats:styled-content>\n                    interneurons could be related to their sparsity of excitatory synaptic inputs compared with\n                    <jats:styled-content style=\"fixed-case\">FSI<\/jats:styled-content>\n                    s. However, in symptomatic mice, a subpopulation of\n                    <jats:styled-content style=\"fixed-case\">LTS<\/jats:styled-content>\n                    interneurons displayed an increase in action potential firing within oscillating bursts. Thus, we conclude that while both\n                    <jats:styled-content style=\"fixed-case\">FSI<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">LTS<\/jats:styled-content>\n                    interneurons demonstrate increases in excitability, the\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    mutation differentially affects their membrane and synaptic properties as well as their ability to respond to compensatory challenges presented during the late stage of the disease. Alterations in\n                    <jats:styled-content style=\"fixed-case\">GABA<\/jats:styled-content>\n                    ergic interneuron intrinsic activity and responsiveness to incoming signals may significantly affect\n                    <jats:styled-content style=\"fixed-case\">SPN<\/jats:styled-content>\n                    output thus contributing to abnormal motor movements in patients afflicted with\n                    <jats:styled-content style=\"fixed-case\">HD<\/jats:styled-content>\n                    .\n                  <\/jats:p>","DOI":"10.1111\/ejn.14283","type":"journal-article","created":{"date-parts":[[2018,11,25]],"date-time":"2018-11-25T04:05:12Z","timestamp":1543118712000},"page":"79-93","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Striatal\n                    <scp>GABA<\/scp>\n                    ergic interneuron dysfunction in the Q175 mouse model of Huntington's disease"],"prefix":"10.1111","volume":"49","author":[{"given":"Sandra M.","family":"Holley","sequence":"first","affiliation":[{"name":"Intellectual and Developmental Disabilities Research Center Department of Psychiatry and Biobehavioral Sciences Semel Institute for Neuroscience and Human Behavior Brain Research Institute UCLA  Los Angeles California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laurie","family":"Galvan","sequence":"additional","affiliation":[{"name":"Intellectual and Developmental Disabilities Research Center Department of Psychiatry and Biobehavioral Sciences Semel Institute for Neuroscience and Human Behavior Brain Research Institute UCLA  Los Angeles California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Talia","family":"Kamdjou","sequence":"additional","affiliation":[{"name":"Intellectual and Developmental Disabilities Research Center Department of Psychiatry and Biobehavioral Sciences Semel Institute for Neuroscience and Human Behavior Brain Research Institute UCLA  Los Angeles California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carlos","family":"Cepeda","sequence":"additional","affiliation":[{"name":"Intellectual and Developmental Disabilities Research Center Department of Psychiatry and Biobehavioral Sciences Semel Institute for Neuroscience and Human Behavior Brain Research Institute UCLA  Los Angeles California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8681-204X","authenticated-orcid":false,"given":"Michael S.","family":"Levine","sequence":"additional","affiliation":[{"name":"Intellectual and Developmental Disabilities Research Center Department of Psychiatry and Biobehavioral Sciences Semel Institute for Neuroscience and Human Behavior Brain Research Institute UCLA  Los Angeles California"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2018,12,10]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3539-10.2011"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1002\/(ISSN)1531-8249"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/nature02998"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.3354-17.2018"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/ejn.13881"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrdp.2015.5"},{"key":"e_1_2_10_8_1","volume-title":"Huntington's disease","author":"Bates 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