{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T13:38:40Z","timestamp":1783690720533,"version":"3.55.0"},"reference-count":24,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2020,8,27]],"date-time":"2020-08-27T00:00:00Z","timestamp":1598486400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["F32NS093813"],"award-info":[{"award-number":["F32NS093813"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["NS096994"],"award-info":[{"award-number":["NS096994"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["NS41574"],"award-info":[{"award-number":["NS41574"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2020,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    In Huntington's disease (HD), the output of striatal indirect pathway medium\u2010sized spiny neurons (MSNs) is altered in its target region, the external globus pallidus (GPe). In a previous study we demonstrated that selective optogenetic stimulation of indirect pathway MSNs induced prolonged decay time of \u03b3\u2010aminobutyric acid (GABA) responses in GPe neurons. Here we identified the mechanism underlying this alteration. Electrophysiological recordings in slices from symptomatic R6\/2 and wildtype (WT) mice were used to evaluate, primarily, the effects of GABA transporter (GAT) antagonists on responses evoked by optogenetic activation of indirect pathway MSNs. In addition, immunohistochemistry (IHC) and Western blots (WBs) were used to examine GAT\u20103 expression in HD and WT mice. A GAT\u20103 blocker (SNAP5114) increased decay time of GABA responses in WT and HD GPe neurons, but the effect was significantly greater in WT neurons. In contrast, a GAT\u20101 antagonist (NO\u2010711) or a GABA\n                    <jats:sub>B<\/jats:sub>\n                    receptor antagonist (CGP 54626) produced small increases in decay time but no differential effects between genotypes. IHC and WBs showed reduction of GAT\u20103 expression in the GPe of HD mice. Thus, reduced expression or dysfunction of GAT\u20103 could underlie alterations of GPe responses to GABA inputs from striatum and could be a target for therapeutic intervention.\n                  <\/jats:p>","DOI":"10.1002\/jnr.24710","type":"journal-article","created":{"date-parts":[[2020,8,28]],"date-time":"2020-08-28T10:45:07Z","timestamp":1598611507000},"page":"2349-2356","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":10,"title":["Mechanisms underlying the enhancement of \u03b3\u2010aminobutyric acid responses in the external globus pallidus of R6\/2 Huntington\u2019s disease model mice"],"prefix":"10.1002","volume":"98","author":[{"given":"Joshua","family":"Barry","sequence":"first","affiliation":[{"name":"IDDRC, Jane and Terry Semel Institute for Neuroscience &amp; Human Behavior David Geffen School of Medicine University of California Los Angeles Los Angeles CA 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