ArticleFrontiers in neural circuits2013
Reduced tonic inhibition in striatal output neurons from Huntington mice due to loss of astrocytic GABA release through GAT-3.
Article in Frontiers in neural circuits, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 104 citations in OpenAlex.
- Glial-neuronal crosstalk via GABA signaling: mechanistic insights into neuropsychiatric and neurological pathophysiology.Molecular psychiatry · 2026Review
- The effect of astrocyte depletion and repopulation approaches in pathological condition of CNS.Acta neurologica Belgica · 2026Review
- Astrocyte-neuron combined targeting for CYP46A1 gene therapy in Huntington's disease.Acta neuropathologica communications · 2025Article
- Unveiling the role of Na⁺/K⁺-ATPase pump: neurodegenerative mechanisms and therapeutic horizons.Pharmacological reports : PR · 2025Review
- Clinical efficacy and potential mechanisms of acupuncture for Parkinson's disease: the role of GABAergic signaling.Frontiers in neuroscience · 2025Review
- Modulation of SNARE-dependent exocytosis in astrocytes improves neuropathology in Huntington's disease.Disease models & mechanisms · 2024Article
- GABA co-released from striatal dopamine axons dampens phasic dopamine release through autoregulatory GABACell reports · 2024Article
- Article
- Astrocytic contributions to Huntington's disease pathophysiology.Annals of the New York Academy of Sciences · 2023Review
- Astrocyte regulation of synaptic signaling in psychiatric disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Review
- 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
- A comparative review on the well-studied GAT1 and the understudied BGT-1 in the brain.Frontiers in physiology · 2023Review
- GABA Release from Astrocytes in Health and Disease.International journal of molecular sciences · 2022Review
- The role of NaCNS neuroscience & therapeutics · 2022Review
- Putrescine Intensifies Glu/GABA Exchange Mechanism and Promotes Early Termination of Seizures.International journal of molecular sciences · 2022Article
- Synaptic Dysfunction in Huntington's Disease: Lessons from Genetic Animal Models.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2022Article
- Astrocytes: GABAceptive and GABAergic Cells in the Brain.Frontiers in cellular neuroscience · 2022Review
- Alzheimer's Disease Enhanced Tonic Inhibition is Correlated With Upregulated Astrocyte GABA Transporter-3/4 in a Knock-InFrontiers in pharmacology · 2022Article
- Neuroinflammation in Huntington's Disease: A Starring Role for Astrocyte and Microglia.Current neuropharmacology · 2022Review
- Astrocyte-neuron interaction in the dorsal striatum-pallidal circuits and alcohol-seeking behaviors.Neuropharmacology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The extracellular concentration of the two main neurotransmitters glutamate and GABA is low but not negligible which enables a number of tonic actions. The effects of ambient GABA vary in a region-, cell-type, and age-dependent manner and can serve as indicators of disease-related alterations. Here we explored the tonic inhibitory actions of GABA in Huntington's disease (HD). HD is a devastating neurodegenerative disorder caused by a mutation in the huntingtin gene. Whole cell patch clamp recordings from striatal output neurons (SONs) in slices from adult wild type mice and two mouse models of HD (Z_Q175_KI homozygotes or R6/2 heterozygotes) revealed an HD-related reduction of the GABA(A) receptor-mediated tonic chloride current (I(Tonic(GABA))) along with signs of reduced GABA(B) receptor-mediated presynaptic depression of synaptic GABA release. About half of I(Tonic(GABA)) depended on tetrodotoxin-sensitive synaptic GABA release, but the remaining current was still lower in HD. Both in WT and HD, I(Tonic(GABA)) was more prominent during the first 4 h after preparing the slices, when astrocytes but not neurons exhibited a transient depolarization. All further tests were performed within 1-4 h in vitro. Experiments with SNAP5114, a blocker of the astrocytic GABA transporter GAT-3, suggest that in WT but not HD GAT-3 operated in the releasing mode. Application of a transportable substrate for glutamate transporters (D-aspartate 0.1-1 mM) restored the non-synaptic GABA release in slices from HD mice. I(Tonic(GABA)) was also rescued by applying the hyperagonist gaboxadol (0.33 μM). The results lead to the hypothesis that lesion-induced astrocyte depolarization facilitates non-synaptic release of GABA through GAT-3. However, the capacity of depolarized astrocytes to provide GABA for tonic inhibition is strongly reduced in HD.
Indexed as
Identifiers
What OpenQuestion holds
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.