ArticleScientific reports2016
Inhibition promotes long-term potentiation at cerebellar excitatory synapses.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- The Effect of taVNS on the Cerebello-Thalamo-Cortical Pathway: a TMS Study.Cerebellum (London, England) · 2024Trial
- HCAR1-mediated lactate signaling modulates motor behavior and regulates spontaneous firing in Purkinje cells.iScience · 2026Article
- Prenatal cannabinoid exposure alters excitation-inhibition balance through glutamate and GABA receptor-mediated signaling.The Journal of biological chemistry · 2026Article
- GABA, Glx, and GSH in the cerebellum: their role in motor performance and learning across age groups.Frontiers in aging neuroscience · 2025Article
- Article
- Intrinsic plasticity of Purkinje cell serves homeostatic regulation of fear memory.Molecular psychiatry · 2024Article
- Excitation and Inhibition Delays within a Feedforward Inhibitory Pathway Modulate Cerebellar Purkinje Cell Output in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Ghrelin signaling in the cerebellar cortex enhances GABAergic transmission onto Purkinje cells.Scientific reports · 2023Article
- Expression Pattern of T-Type CaCells · 2021Article
- Article
- Cerebellar Development and Circuit Maturation: A Common Framework for Spinocerebellar Ataxias.Frontiers in neuroscience · 2020Review
- Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of the cerebellar cortex to learn from experience ensures the accuracy of movements and reflex adaptation, processes which require long-term plasticity at granule cell (GC) to Purkinje neuron (PN) excitatory synapses. PNs also receive GABAergic inhibitory inputs via GCs activation of interneurons; despite the involvement of inhibition in motor learning, its role in long-term plasticity is poorly characterized. Here we reveal a functional coupling between ionotropic GABAA receptors and low threshold CaV3 calcium channels in PNs that sustains calcium influx and promotes long-term potentiation (LTP) at GC to PN synapses. High frequency stimulation induces LTP at GC to PN synapses and CaV3-mediated calcium influx provided that inhibition is intact; LTP is mGluR1, intracellular calcium store and CaV3 dependent. LTP is impaired in CaV3.1 knockout mice but it is nevertheless recovered by strengthening inhibitory transmission onto PNs; promoting a stronger hyperpolarization via GABAA receptor activation leads to an enhanced availability of an alternative Purkinje-expressed CaV3 isoform compensating for the lack of CaV3.1 and restoring LTP. Accordingly, a stronger hyperpolarization also restores CaV3-mediated calcium influx in PNs from CaV3.1 knockout mice. We conclude that by favoring CaV3 channels availability inhibition promotes LTP at cerebellar excitatory synapses.
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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.