ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Enhancement of GABA release through endogenous activation of axonal GABA(A) receptors in juvenile cerebellum.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- Differentially poised vesicles underlie fast and slow components of release at single synapses.The Journal of general physiology · 2020Article
- Incomplete vesicular docking limits synaptic strength under high release probability conditions.eLife · 2020Article
- Axonal GABAThe Journal of physiology · 2017Article
- Action potential broadening in a presynaptic channelopathy.Nature communications · 2016Article
- Impact of single-site axonal GABAergic synaptic events on cerebellar interneuron activity.The Journal of general physiology · 2015Article
- Transmembrane AMPAR regulatory protein γ-2 is required for the modulation of GABA release by presynaptic AMPARs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Long-term inhibitory plasticity in visual cortical layer 4 switches sign at the opening of the critical period.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Enhanced inhibitory neurotransmission in the cerebellar cortex of Atp1a3-deficient heterozygous mice.The Journal of physiology · 2013Article
- GABAA receptors increase excitability and conduction velocity of cerebellar parallel fiber axons.Journal of neurophysiology · 2012Article
- Ionotropic receptors at hippocampal mossy fibers: roles in axonal excitability, synaptic transmission, and plasticity.Frontiers in neural circuits · 2012Article
- Somatic depolarization enhances GABA release in cerebellar interneurons via a calcium/protein kinase C pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Clinical profile of vigabatrin as monotherapy for treatment of infantile spasms.Neuropsychiatric disease and treatment · 2010Article
- Presynaptic GABAA receptors enhance transmission and LTP induction at hippocampal mossy fiber synapses.Nature neuroscience · 2010Article
- Nerve Terminal GABAA Receptors Activate Ca2+/Calmodulin-dependent Signaling to Inhibit Voltage-gated Ca2+ Influx and Glutamate Release.The Journal of biological chemistry · 2009Article
- Impaired GABAergic transmission disrupts normal homeostatic plasticity in rat cortical networks.The European journal of neuroscience · 2008Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence indicates the presence of presynaptic GABA(A) receptors (GABA(A)Rs) in the axon domain of several classes of central neurons, including cerebellar basket and stellate cells. Here, we investigate the possibility that these receptors could be activated in the absence of electrical or chemical stimulation. We find that low concentrations of GABA increase the frequency of miniature GABAergic synaptic currents. Submaximal concentrations of a GABA(A)R blocker, gabazine, decrease both the miniature current frequency and the probability of evoked GABA release. Zolpidem, an agonist of the benzodiazepine binding site, and NO-711 (1-[2-[[(diphenylmethylene)imino]oxy]ethyl]-1,2,5,6-tetrahydro-3-pyridinecarboxylic acid hydrochloride), a blocker of GABA uptake, both increase the frequency of miniature currents. These effects occur up to postnatal day 14, but not later. Immunohistochemistry indicates the presence of alpha1-containing GABA(A)Rs in interneuron presynaptic terminals with a similar age dependence. We conclude that, under resting conditions, axonal GABA(A)Rs are significantly activated, that this activation results in enhanced GABA release, and that it can be augmented by increasing the affinity of GABA(A)Rs or reducing GABA uptake. Our findings suggest the existence of a positive-feedback mechanism involving presynaptic GABA(A)Rs that maintains a high release rate and a high local GABA concentration in the immature cerebellar network.
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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.