ArticleJournal of neuroscience research2020
Mechanisms underlying the enhancement of γ-aminobutyric acid responses in the external globus pallidus of R6/2 Huntington's disease model mice.
Article in Journal of neuroscience research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 8 citations in OpenAlex.
- Bidirectional communication between the gut microbiota and the central nervous system.Neural regeneration research · 2026Article
- Hippocampal astrocytic GAT-3 blockade impairs protein synthesis and spatial memory dynamics.Communications biology · 2026Article
- Restoring Compromised ClThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Application of Optogenetics in Neurodegenerative Diseases.Cellular and molecular neurobiology · 2024Review
- Correlation between the gut microbiome and neurodegenerative diseases: a review of metagenomics evidence.Neural regeneration research · 2024Review
- A bibliometric profile of optogenetics: quantitative and qualitative analyses.Frontiers in neuroscience · 2023Article
- Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Article
- Synaptic pathology in Huntington's disease: Beyond the corticostriatal pathway.Neurobiology of disease · 2022Review
- A Brief History and the Significance of the GABACurrent topics in behavioral neurosciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
In Huntington's disease (HD), the output of striatal indirect pathway medium-sized 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 γ-aminobutyric 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-3 expression in HD and WT mice. A GAT-3 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-1 antagonist (NO-711) or a GABA
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Registered trials
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