ArticleFrontiers in molecular neuroscience2017
Differential Alteration in Expression of Striatal GABA
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Re-Evaluation of the Ultrastructural Localization of Tonic GABA-A Receptors.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Altered Inhibitory Synaptic Transmission and Changes in GABAergic Markers in the Hippocampus of Genetic and Environmental Animal Model of Autism.Neurochemical research · 2025Article
- Altered GABAergic Homeostasis in the Striatum of Dopamine Transporter Knockout Rats.Current neuropharmacology · 2025Article
- Restoring Compromised ClThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Shank3 deficiency alters midbrain GABAergic neuron morphology, GABAergic markers and synaptic activity in primary striatal neurons.Molecular brain · 2024Article
- Neurotrophins and Their Receptors: BDNF's Role in GABAergic Neurodevelopment and Disease.International journal of molecular sciences · 2024Review
- Shank3 Deficiency Results in a Reduction in GABAergic Postsynaptic Puncta in the Olfactory Brain Areas.Neurochemical research · 2024Article
- Extracellular vesicles improve GABAergic transmission in Huntington's disease iPSC-derived neurons.Theranostics · 2023Article
- Altered exocytosis of inhibitory synaptic vesicles at single presynaptic terminals of cultured striatal neurons in a knock-in mouse model of Huntington's disease.Frontiers in molecular neuroscience · 2023Article
- Molecular Pathophysiological Mechanisms in Huntington's Disease.Biomedicines · 2022Review
- Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Article
- Shank3 Deficiency is Associated With Altered Profile of Neurotransmission Markers in Pups and Adult Mice.Neurochemical research · 2021Article
- Striatal Chloride Dysregulation and Impaired GABAergic Signaling Due to Cation-Chloride Cotransporter Dysfunction in Huntington's Disease.Frontiers in cellular neuroscience · 2021Review
- Enhanced GABAergic Inhibition of Cholinergic Interneurons in the zQ175Frontiers in systems neuroscience · 2020Article
- Major Contribution of Somatostatin-Expressing Interneurons and Cannabinoid Receptors to Increased GABA Synaptic Activity in the Striatum of Huntington's Disease Mice.Frontiers in synaptic neuroscience · 2019Article
- Striatal Neurodegeneration that Mimics Huntington's Disease Modifies GABA-induced Currents.Brain sciences · 2018Article
- Insights into GABAOpen biology · 2018Review
- The TinyInternational journal of molecular sciences · 2018Review
- Striatal Direct and Indirect Pathway Output Structures Are Differentially Altered in Mouse Models of Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- The adjustment of γ-aminobutyric acidNeural regeneration research · 2018Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Huntington's disease (HD) is a neurodegenerative disorder characterized by progressive motor symptoms that are preceded by cognitive deficits and is considered as a disorder that primarily affects forebrain striatal neurons. To gain a better understanding of the molecular and cellular mechanisms associated with disease progression, we analyzed the expression of proteins involved in GABAergic neurotransmission in the striatum of the R6/1 transgenic mouse model. Western blot, quantitative PCR and immunohistochemical analyses were conducted on male R6/1 mice and age-matched wild type littermates. Analyses were performed on 2 and 6 month-old animals, respectively, before and after the onset of motor symptoms. Expression of GAD 67, GAD 65, NL2, or gephyrin proteins, involved in GABA synthesis or synapse formation did not display major changes. In contrast, expression of α1, α3 and α5 GABA
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.