ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Axonal GABAA receptors increase cerebellar granule cell excitability and synaptic activity.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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
54 citing papers in PubMed, 84 citations in OpenAlex.
- High-frequency axonal bursts mediate bidirectional modulation of dopamine signaling by nicotinic receptors.bioRxiv : the preprint server for biology · 2026Article
- Beyond synaptic plasticity: a summary of a linear model of the cerebellar locomotor computation.Frontiers in neural circuits · 2026Review
- Co-release of GABA and ACh from Medial Olivocochlear Neurons as a Fine Regulatory Mechanism of Cochlear Efferent Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- GABAergic synapses between auditory efferent neurons and type II spiral ganglion afferent neurons in the mouse cochlea.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Computational anatomy: the cerebellar microzone computation.Oxford open neuroscience · 2025Article
- Intrinsic and synaptic regulation of axonal excitability in dopaminergic neurons.Frontiers in cellular neuroscience · 2025Review
- Co-release of GABA and ACh from medial olivocochlear neurons fine tunes cochlear efferent inhibition.bioRxiv : the preprint server for biology · 2024Article
- Activity-Dependent Ectopic Spiking in Parvalbumin-Expressing Interneurons of the Neocortex.eNeuro · 2024Article
- Distinct GABAergic modulation of timing-dependent LTP in CA1 pyramidal neurons along the longitudinal axis of the mouse hippocampus.iScience · 2024Article
- Interplay between metabotropic glutamate type 4 and adenosine type 1 receptors modulate synaptic transmission in the cerebellar cortex.Frontiers in pharmacology · 2024Article
- Bumetanide Attenuates Cognitive Deficits and Brain Damage in Rats Subjected to Hypoxia-Ischemia at Two Time Points of the Early Postnatal Period.Neurotoxicity research · 2023Article
- Aion is a bistable anion-conducting channelrhodopsin that provides temporally extended and reversible neuronal silencing.Communications biology · 2022Article
- Mechanisms and Consequences of Cerebellar Purkinje Cell Disinhibition in a Mouse Model of Duchenne Muscular Dystrophy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Noradrenergic terminal short-term potentiation enables modality-selective integration of sensory input and vigilance state.Science advances · 2021Article
- Axonal Modulation of Striatal Dopamine Release by Local γ-Aminobutyric Acid (GABA) Signalling.Cells · 2021Review
- Article
- Direction of action of presynaptic GABAJournal of neurophysiology · 2019Article
- Antidromic Analog Signaling.Frontiers in cellular neuroscience · 2019Review
- Reciprocal Regulation of KCC2 Trafficking and Synaptic Activity.Frontiers in cellular neuroscience · 2019Review
- High-efficiency optogenetic silencing with soma-targeted anion-conducting channelrhodopsins.Nature communications · 2018Article
Corrections and comments
- Commented on by
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
We report that activation of GABA(A) receptors on cerebellar granule cell axons modulates both transmitter release and the excitability of the axon and soma. Axonal GABA(A) receptors depolarize the axon, increasing its excitability and causing calcium influx at axonal varicosities. GABA-mediated subthreshold depolarizations in the axon spread electrotonically to the soma, promoting orthodromic action potential initiation. When chloride concentrations are unperturbed, GABA iontophoresis elicits spikes and increases excitability of parallel fibers, indicating that GABA(A) receptor-mediated responses are normally depolarizing. GABA release from molecular layer interneurons activates parallel fiber GABA(A) receptors, and this, in turn, increases release probability at synapses between parallel fibers and molecular layer interneurons. These results describe a positive feedback mechanism whereby transmission from granule cells to Purkinje cells and molecular layer interneurons will be strengthened during granule cell spike bursts evoked by sensory stimulation.
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.