ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Short-term depression at the reciprocal synapses between a retinal bipolar cell terminal and amacrine cells.
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 24 papers.
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Who cites it
24 citing papers in PubMed, 30 citations in OpenAlex.
- Short-term plasticity and context-dependent circuit function: Insights from retinal circuitry.Science advances · 2024Review
- Temporal pattern recognition in retinal ganglion cells is mediated by dynamical inhibitory synapses.Nature communications · 2024Article
- The Impact of Multivesicular Release on the Transmission of Sensory Information by Ribbon Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- A theoretical model reveals specialized synaptic depressions and temporal frequency tuning in retinal parallel channels.Frontiers in computational neuroscience · 2022Article
- Glycine Release Is Potentiated by cAMP via EPAC2 and CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Diversity in spatial scope of contrast adaptation among mouse retinal ganglion cells.Journal of neurophysiology · 2017Article
- Building blocks of temporal filters in retinal synapses.PLoS biology · 2014Article
- A synaptic mechanism for temporal filtering of visual signals.PLoS biology · 2014Article
- Nonlinear spatial integration in the receptive field surround of retinal ganglion cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Glycine transporter 1 modulates GABA release from amacrine cells by controlling occupancy of coagonist binding site of NMDA receptors.Journal of neurophysiology · 2013Article
- Independent control of reciprocal and lateral inhibition at the axon terminal of retinal bipolar cells.The Journal of physiology · 2013Article
- Spatial segregation of adaptation and predictive sensitization in retinal ganglion cells.Neuron · 2013Article
- Slow changes in Ca2(+) cause prolonged release from GABAergic retinal amacrine cells.Journal of neurophysiology · 2013Article
- Paired-pulse plasticity in the strength and latency of light-evoked lateral inhibition to retinal bipolar cell terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Light-evoked lateral GABAergic inhibition at single bipolar cell synaptic terminals is driven by distinct retinal microcircuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Nonlinear interactions between excitatory and inhibitory retinal synapses control visual output.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Coordinated dynamic encoding in the retina using opposing forms of plasticity.Nature neuroscience · 2011Article
- A synaptic mechanism for retinal adaptation to luminance and contrast.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Multiple pathways of inhibition shape bipolar cell responses in the retina.Visual neuroscience · 2011Review
- Pharmacological analysis of the activation and receptor properties of the tonic GABA(C)R current in retinal bipolar cell terminals.PloS one · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Visual adaptation is thought to occur partly at retinal synapses that are subject to plastic changes. However, the locus and properties of this plasticity are not well known. Here, we studied short-term plasticity at the reciprocal synapse between bipolar cell terminals and amacrine cells in goldfish retinal slices. Depolarization of a single bipolar cell terminal for 100 ms triggers the release of glutamate onto amacrine cell processes, which in turn leads to GABAergic feedback from amacrine cells onto the same terminal. We find that this release of GABA undergoes paired-pulse depression (PPD) that recovers in <1 min (single exponential time constant, tau approximately = 12 s). This disynaptic PPD is independent of mGluR-mediated plasticity and depletion of glutamatergic synaptic vesicle pools, because exocytosis assayed via capacitance jumps (deltaC(m)) recovered completely after 10 s (tau approximately = 2 s). Fast application of GABA (10 mM) onto outside-out patches excised from bipolar cell terminals showed that the recovery of GABA(A) receptors from desensitization depends on the duration of the application [fast recovery (<2 s) for short applications; slow (tau approximately = 12 s) for prolonged applications]. We thus blocked GABA(A) receptors and retested the GABAergic response mediated by nondesensitizing GABA(C) receptors to two rapid glutamate puffs onto the bipolar cell terminal. These responses consistently displayed PPD. Furthermore, blocking AMPA-receptor desensitization with cyclothiazide, or evoking GABA release with NMDA receptors, did not reduce PPD. We thus suggest that depletion of synaptic vesicle pools in GABAergic amacrine cells is a major contributor to PPD.
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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.