Synaptic release at mammalian bipolar cell terminals

Wan, Qun; Heidelberger, Ruth

doi:10.1017/s0952523810000453

Cited by 34 publications

(38 citation statements)

References 156 publications

(344 reference statements)

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“…Examples include bipolar cells with rectification and synaptic depression in their axon terminal [74–76] as well as different types of amacrine cells that veto ganglion cell response when specific visual features are present [68, 77–80]. Given the extreme diversity of amacrine cell types [81] as well as the fact that they can individually remold each bipolar-to-ganglion cell transfer function [82], the prospect for deriving an input-output model that will succeed over the entire range of natural visual conditions currently seems quite remote.…”

Section: Discussionmentioning

confidence: 99%

Error-Robust Modes of the Retinal Population Code

et al. 2016

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Across the nervous system, certain population spiking patterns are observed far more frequently than others. A hypothesis about this structure is that these collective activity patterns function as population codewords–collective modes–carrying information distinct from that of any single cell. We investigate this phenomenon in recordings of ∼150 retinal ganglion cells, the retina’s output. We develop a novel statistical model that decomposes the population response into modes; it predicts the distribution of spiking activity in the ganglion cell population with high accuracy. We found that the modes represent localized features of the visual stimulus that are distinct from the features represented by single neurons. Modes form clusters of activity states that are readily discriminated from one another. When we repeated the same visual stimulus, we found that the same mode was robustly elicited. These results suggest that retinal ganglion cells’ collective signaling is endowed with a form of error-correcting code–a principle that may hold in brain areas beyond retina.

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Section: Discussionmentioning

confidence: 99%

Error-Robust Modes of the Retinal Population Code

et al. 2016

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“…The PA-generating properties of RIBEYE suggest that PA fulfils essential roles in synaptic ribbondependent vesicle trafficking. Intense exocytic and endocytic membrane trafficking occurs at synaptic ribbons (Schmitz, 2009;Wan and Heidelberger, 2011). Based on its well-known role in neuroendocrine cells (Bader and Vitale, 2009), it is tempting to assume that PA directly facilitates synaptic vesicle fusion also in ribbon synapses.…”

Section: Ribeye Is a Palmitoyl-coa-dependent Lpa Acyltransferase Thatmentioning

confidence: 99%

“…They are characterized by high rates of synaptic vesicle exocytosis, coordinated multivesicular release, and exquisite sensitivity over a wide dynamic range of signaling, including both phasic and tonic components (Wan and Heidelberger, 2011). The main site of exocytosis is characterized by unique presynaptic structures, the synaptic ribbons, which are associated with large numbers of synaptic vesicles.…”

Section: Introductionmentioning

confidence: 99%

“…Thus, synaptic ribbons are crucial for signaling at these types of synapses (Schmitz, 2009;Meyer and Moser, 2010;Wan and Heidelberger, 2011), but the detailed mechanisms how ribbons perform these functions remain elusive. RIBEYE (RE) is a protein specific to synaptic ribbons and, consequently, thought to be a major determinant of ribbon function (Schmitz et al, 2000;Magupalli et al, 2008;Schmitz, 2009).…”

Section: Introductionmentioning

confidence: 99%

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The Synaptic Ribbon Is a Site of Phosphatidic Acid Generation in Ribbon Synapses

Schwarz¹,

Natarajan²,

Kassas³

et al. 2011

J. Neurosci.

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Ribbon synapses continuously transmit graded membrane potential changes into changes of synaptic vesicle exocytosis and rely on intense synaptic membrane trafficking. The synaptic ribbon is considered central to this process. In the present study we asked whether tonically active ribbon synapses are associated with the generation of certain lipids, specifically the highly active signaling phospholipid phosphatidic acid (PA). Using PA-sensor proteins, we demonstrate that PA is enriched at mouse retinal ribbon synapses in close vicinity to the synaptic ribbon in situ. As shown by heterologous expression, RIBEYE, a main component of synaptic ribbons, is responsible for PA binding at synaptic ribbons. Furthermore, RIBEYE is directly involved in the synthesis of PA. Using various independent substrate binding and enzyme assays, we demonstrate that the B domain of RIBEYE possesses lysophosphatidic acid (LPA) acyltransferase (LPAAT) activity, which leads to the generation of PA from LPA. Since an LPAAT-deficient RIBEYE mutant does not recruit PA-binding proteins to artificial synaptic ribbons, whereas wild-type RIBEYE supports PA binding, we conclude that the LPAAT activity of the RIBEYE(B) domain is a physiologically relevant source of PA generation at the synaptic ribbon. We propose that PA generated at synaptic ribbons likely facilitates synaptic vesicle trafficking.

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“…However, ganglion cell spike encoding is dynamically modulated by two-types of inhibitory interneurons: horizontal and amacrine cells (Masland, 2012). Bipolar cell synapses contain specialized ribbon-type active zones, which can release glutamate at high rates (Snellman et al, 2009; Wan and Heidelberger, 2011). Interestingly, the postsynaptic sites of these ribbon synapses often express Ca 2+ -permeable AMPA receptors (CP-AMPARs), which presumably signal the high rates of glutamate release from bipolar cells (Osswald et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Postsynaptic Plasticity Triggered by Ca2+-Permeable AMPA Receptor Activation in Retinal Amacrine Cells

Kim

Gersdorff

2016

Neuron

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SUMMARY Amacrine cells are thought to be a major locus for mechanisms of light adaptation and contrast enhancement in the retina. However, the potential for plasticity in their AMPA receptor currents remains largely unknown. Using paired patch-clamp recordings between bipolar cell terminals and amacrine cells, we have simultaneously measured presynaptic membrane capacitance changes and EPSCs. Repetitive bipolar cell depolarizations, designed to maintain the same amount of exocytosis, nevertheless significantly potentiated evoked EPSCs in a subpopulation of amacrine cells. Likewise, repetitive iontophoresis (or puffs) of glutamate (or AMPA) onto the dendrites of amacrine cells also significantly potentiated evoked currents and [Ca2+]i rises. However, strong postsynaptic Ca2+ buffering with BAPTA abolished the potentiation and selective antagonists of Ca2+-permeable AMPA receptors also blocked the potentiation of AMPA-mediated currents. Together these results suggest that Ca2+ influx via Ca2+-permeable AMPA receptors can elicit a rapid form of postsynaptic plasticity in a subgroup of amacrine cell dendrites.

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Synaptic release at mammalian bipolar cell terminals

Cited by 34 publications

References 156 publications

Error-Robust Modes of the Retinal Population Code

Error-Robust Modes of the Retinal Population Code

The Synaptic Ribbon Is a Site of Phosphatidic Acid Generation in Ribbon Synapses

Postsynaptic Plasticity Triggered by Ca2+-Permeable AMPA Receptor Activation in Retinal Amacrine Cells

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