ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
At immature mossy-fiber-CA3 synapses, correlated presynaptic and postsynaptic activity persistently enhances GABA release and network excitability via BDNF and cAMP-dependent PKA.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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46 citing papers in PubMed, 82 citations in OpenAlex.
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- Advances in the Electrophysiological Recordings of Long-Term Potentiation.International journal of molecular sciences · 2023Review
- Impaired synaptic plasticity in an animal model of autism exhibiting early hippocampal GABAergic-BDNF/TrkB signaling alterations.iScience · 2023Article
- Brain is modulated by neuronal plasticity during postnatal development.The journal of physiological sciences : JPS · 2021Review
- The ins and outs of inhibitory synaptic plasticity: Neuron types, molecular mechanisms and functional roles.The European journal of neuroscience · 2021Review
- CCL2/CCR2 Contributes to the Altered Excitatory-inhibitory Synaptic Balance in the Nucleus Accumbens Shell Following Peripheral Nerve Injury-induced Neuropathic Pain.Neuroscience bulletin · 2021Article
- Long-term depression at hippocampal mossy fiber-CA3 synapses involves BDNF but is not mediated by p75NTR signaling.Scientific reports · 2021Article
- Dysregulation of GABAergic Signaling in Neurodevelomental Disorders: Targeting Cation-Chloride Co-transporters to Re-establish a Proper E/I Balance.Frontiers in cellular neuroscience · 2021Review
- Immature Dentate Granule Cells Require Ntrk2/Trkb for the Formation of Functional Hippocampal Circuitry.iScience · 2020Article
- Inhibitory Plasticity: From Molecules to Computation and Beyond.International journal of molecular sciences · 2020Review
- Preserving the balance: diverse forms of long-term GABAergic synaptic plasticity.Nature reviews. Neuroscience · 2019Review
- Hebbian Spike-Timing Dependent Plasticity at the Cerebellar Input Stage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Article
- Coexistence of Multiple Types of Synaptic Plasticity in Individual Hippocampal CA1 Pyramidal Neurons.Frontiers in synaptic neuroscience · 2017Article
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- Ethanol exposure during the third trimester equivalent does not affect GABAA or AMPA receptor-mediated spontaneous synaptic transmission in rat CA3 pyramidal neurons.Journal of negative results in biomedicine · 2015Article
- A novel form of synaptic plasticity in field CA3 of hippocampus requires GPER1 activation and BDNF release.The Journal of cell biology · 2015Article
- Extracellular proteolysis in structural and functional plasticity of mossy fiber synapses in hippocampus.Frontiers in cellular neuroscience · 2015Review
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the adult rat hippocampus, the axons of granule cells in the dentate gyrus, the mossy fibers (MF), form excitatory glutamatergic synapses with CA3 principal cells. In neonates, MF release into their targets mainly GABA, which at this developmental stage is depolarizing. Here we tested the hypothesis that, at immature MF-CA3 synapses, correlated presynaptic [single fiber-evoked GABA(A)-mediated postsynaptic potentials (GPSPs)] and postsynaptic activity (back propagating action potentials) may exert a critical control on synaptic efficacy. This form of plasticity, called spike-timing-dependent plasticity (STDP), is a Hebbian type form of learning extensively studied at the level of glutamatergic synapses. Depending on the relative timing, pairing postsynaptic spiking and single MF-GPSPs induced bidirectional changes in synaptic efficacy. In case of positive pairing, spike-timing-dependent-long-term potentiation (STD-LTP) was associated with a persistent increase in GPSP slope and in the probability of cell firing. The transduction pathway involved a rise of calcium in the postsynaptic cell and the combined activity of cAMP-dependent PKA (protein kinase A) and brain-derived neurotrophic factor (BDNF). Retrograde signaling via BDNF and presynaptic TrkB receptors led to a persistent increase in GABA release. In "presynaptically" silent neurons, the enhanced probability of GABA release induced by the pairing protocol, unsilenced these synapses. Shifting E(GABA) from the depolarizing to the hyperpolarizing direction with bumetanide failed to modify synaptic strength. Thus, STD-LTP of GPSPs provides a reliable way to convey information from granule cells to the CA3 associative network at a time when glutamatergic synapses are still poorly developed.
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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.