ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Nerve terminal nicotinic acetylcholine receptors initiate quantal GABA release from perisomatic interneurons by activating axonal T-type (Cav3) Ca²⁺ channels and Ca²⁺ release from stores.
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 55 papers.
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Who cites it
55 citing papers in PubMed, 90 citations in OpenAlex.
- Nicotinic acetylcholine receptors in pain modulation.Frontiers in pharmacology · 2026Review
- CaCell reports · 2025Article
- The Role of Voltage-Gated Calcium Channels in Basal Ganglia Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- Interactions between the Nicotinic and Endocannabinoid Receptors at the Plasma Membrane.Membranes · 2022Review
- T-Type CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Schizophrenia Genomics: Convergence on Synaptic Development, Adult Synaptic Plasticity, or Both?Biological psychiatry · 2022Review
- CaInternational journal of molecular sciences · 2022Review
- Neuromodulatory control of inhibitory network arborization in the developing postnatal neocortex.Science advances · 2022Article
- Article
- Seeking the exclusive binding region of phenylalkylamine derivatives on human T-type calcium channels via homology modeling and molecular dynamics simulation approach.Pharmacology research & perspectives · 2021Article
- Cholinergic Signaling, Neural Excitability, and Epilepsy.Molecules (Basel, Switzerland) · 2021Review
- Enhanced hippocampal type II theta activity AND altered theta architecture in mice lacking the CaScientific reports · 2021Article
- Dysregulation of Neuronal Nicotinic Acetylcholine Receptor-Cholesterol Crosstalk in Autism Spectrum Disorder.Frontiers in molecular neuroscience · 2021Article
- Functions of Presynaptic Voltage-gated Calcium Channels.Function (Oxford, England) · 2021Review
- Activation of nicotinic acetylcholine receptors induces potentiation and synchronization within in vitro hippocampal networks.Journal of neurochemistry · 2020Article
- The mechanisms shaping CA2 pyramidal neuron action potential bursting induced by muscarinic acetylcholine receptor activation.The Journal of general physiology · 2020Article
- Neuromodulation of hippocampal long-term synaptic plasticity.Current opinion in neurobiology · 2019Review
- Hippocampal GABAergic Inhibitory Interneurons.Physiological reviews · 2017Review
- Acetylcholine modulates gamma frequency oscillations in the hippocampus by activation of muscarinic M1 receptors.The European journal of neuroscience · 2017Article
- Nicotine-prevented learning and memory impairment in REM sleep-deprived rat is modulated by DREAM protein in the hippocampus.Brain and behavior · 2017Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Release of conventional neurotransmitters is mainly controlled by calcium (Ca²⁺) influx via high-voltage-activated (HVA), Ca(v)2, channels ("N-, P/Q-, or R-types") that are opened by action potentials. Regulation of transmission by subthreshold depolarizations does occur, but there is little evidence that low-voltage-activated, Ca(v)3 ("T-type"), channels take part. GABA release from cortical perisomatic-targeting interneurons affects numerous physiological processes, and yet its underlying control mechanisms are not fully understood. We investigated whether T-type Ca²⁺ channels are involved in regulating GABA transmission from these cells in rat hippocampal CA1 using a combination of whole-cell voltage-clamp, multiple-fluorescence confocal microscopy, dual-immunolabeling electron-microscopy, and optogenetic methods. We show that Ca(v)3.1, T-type Ca²⁺ channels can be activated by α3β4 nicotinic acetylcholine receptors (nAChRs) that are located on the synaptic regions of the GABAergic perisomatic-targeting interneuronal axons, including the parvalbumin-expressing cells. Asynchronous, quantal GABA release can be triggered by Ca²⁺ influx through presynaptic T-type Ca²⁺ channels, augmented by Ca²⁺ from internal stores, following focal microiontophoretic activation of the α3β4 nAChRs. The resulting GABA release can inhibit pyramidal cells. The T-type Ca²⁺ channel-dependent mechanism is not dependent on, or accompanied by, HVA channel Ca²⁺ influx, and is insensitive to agonists of cannabinoid, μ-opioid, or GABA(B) receptors. It may therefore operate in parallel with the normal HVA-dependent processes. The results reveal new aspects of the regulation of GABA transmission and contribute to a deeper understanding of ACh and nicotine actions in CNS.
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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.