ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Brain-derived neurotrophic factor enhances GABA release probability and nonuniform distribution of N- and P/Q-type channels on release sites of hippocampal inhibitory synapses.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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43 citing papers in PubMed, 97 citations in OpenAlex.
- Review
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- REST/NRSF drives homeostatic plasticity of inhibitory synapses in a target-dependent fashion.eLife · 2021Article
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- Orthopedic surgery-induced cognitive dysfunction is mediated by CX3CL1/R1 signaling.Journal of neuroinflammation · 2021Article
- Effect of Repetitive Passive Movement Before Motor Skill Training on Corticospinal Excitability and Motor Learning Depend on BDNF Polymorphisms.Frontiers in human neuroscience · 2021Article
- Partial Activation of TrkB Receptors Corrects Interneuronal Calcium Channel Dysfunction and Reduces Epileptogenic Activity in Neocortex following Injury.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Cav1.2 channelopathies causing autism: new hallmarks on Timothy syndrome.Pflugers Archiv : European journal of physiology · 2020Review
- Ceftriaxone Treatment Preserves Cortical Inhibitory Interneuron Function via Transient Salvage of GLT-1 in a Rat Traumatic Brain Injury Model.Cerebral cortex (New York, N.Y. : 1991) · 2019Article
- Trkb-IP3 Pathway Mediating Neuroprotection in Rat Hippocampal Neuronal Cell Culture Following Induction of Kainic Acid.The Malaysian journal of medical sciences : MJMS · 2018Article
- Nanodiamonds-induced effects on neuronal firing of mouse hippocampal microcircuits.Scientific reports · 2018Article
- Article
- Impaired GABAOncotarget · 2017Article
- Activation of brain-derived neurotrophic factor-tropomyosin receptor kinase B signaling in the pedunculopontine tegmental nucleus: a novel mechanism for the homeostatic regulation of rapid eye movement sleep.Journal of neurochemistry · 2017Article
- Preserved Function of Afferent Parvalbumin-Positive Perisomatic Inhibitory Synapses of Dentate Granule Cells in Rapidly Kindled Mice.Frontiers in cellular neuroscience · 2017Article
- BDNF-induced presynaptic facilitation of GABAergic transmission in the hippocampus of young adults is dependent of TrkB and adenosine A2A receptors.Purinergic signalling · 2016Article
- Synaptic regulation of affective behaviors; role of BDNF.Neuropharmacology · 2014Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long-lasting exposures to brain-derived neurotrophic factor (BDNF) accelerate the functional maturation of GABAergic transmission in embryonic hippocampal neurons, but the molecular bases of this phenomenon are still debated. Evidence in favor of a postsynaptic site of action has been accumulated, but most of the data support a presynaptic site effect. A crucial issue is whether the enhancement of evoked IPSCs (eIPSCs) induced by BDNF is attributable to an increase in any of the elementary parameters controlling neurosecretion, namely the probability of release, the number of release sites, the readily releasable pool (RRP), and the quantal size. Here, using peak-scaled variance analysis of miniature IPSCs, multiple probability fluctuation analysis, and cumulative amplitude analysis of action potential-evoked postsynaptic currents, we show that BDNF increases release probability and vesicle replenishment with little or no effect on the quantal size, the number of release sites, the RRP, and the Ca2+ dependence of eIPSCs. BDNF treatment changes markedly the distribution of Ca2+ channels controlling neurotransmitter release. It enhances markedly the contribution of N- and P/Q-type channels, which summed to >100% ("supra-additivity"), and deletes the contribution of R-type channels. BDNF accelerates the switch of presynaptic Ca2+ channel distribution from "segregated" to "nonuniform" distribution. This maturation effect was accompanied by an uncovered increased control of N-type channels on paired-pulse depression, otherwise dominated by P/Q-type channels in untreated neurons. Nevertheless, BDNF preserved the fast recovery from depression associated with N-type channels. These novel presynaptic BDNF actions derive mostly from an enhanced overlapping and better colocalization of N- and P/Q-type channels to vesicle release sites.
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