ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Disruption of a neural microcircuit in the rod pathway of the mammalian retina by diabetes mellitus.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Decoding the roles of bipolar, amacrine, and horizontal cells.Handbook of clinical neurology · 2026Review
- Review
- Review
- From Neurotransmission to Retinal Pathophysiology: Unraveling the Role of GABA Receptors in Retinal Disease Progression.Journal of neurochemistry · 2025Review
- Induction of a Müller Glial Cell-Specific Protective Pathway Safeguards the Retina From Diabetes-Induced Damage.Diabetes · 2025Article
- Visual Dysfunction in Diabetes.Annual review of vision science · 2023Review
- Preventable risk factors for type 2 diabetes can be detected using noninvasive spontaneous electroretinogram signals.PloS one · 2023Article
- Dendritic Morphology of an Inhibitory Retinal Interneuron Enables Simultaneous Local and Global Synaptic Integration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Inhibitory inputs to an inhibitory interneuron: Spontaneous postsynaptic currents and GABAThe European journal of neuroscience · 2022Article
- Impaired Light Adaptation of ON-Sustained Ganglion Cells in Early Diabetes Is Attributable to Diminished Response to Dopamine D4 Receptor Activation.Investigative ophthalmology & visual science · 2022Article
- Early Microvascular and Oscillatory Potentials Changes in Human Diabetic Retina: Amacrine Cells and the Intraretinal Neurovascular Crosstalk.Journal of clinical medicine · 2021Article
- An Update on Connexin Gap Junction and Hemichannels in Diabetic Retinopathy.International journal of molecular sciences · 2021Review
- Differential Contribution of Gap Junctions to the Membrane Properties of ON- and OFF-Bipolar Cells of the Rat Retina.Cellular and molecular neurobiology · 2021Article
- The effects of early diabetes on inner retinal neurons.Visual neuroscience · 2020Article
- Reductions in Calcium Signaling Limit Inhibition to Diabetic Retinal Rod Bipolar Cells.Investigative ophthalmology & visual science · 2019Article
- Capacitance measurement of dendritic exocytosis in an electrically coupled inhibitory retinal interneuron: an experimental and computational study.Physiological reports · 2019Article
- Extrasynaptic NMDA Receptors on Rod Pathway Amacrine Cells: Molecular Composition, Activation, and Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- One month of hyperglycemia alters spectral responses of the zebrafish photopic electroretinogram.Disease models & mechanisms · 2018Article
- Bone Marrow CD133Cell transplantation · 2018Article
- Dopamine Deficiency Mediates Early Rod-Driven Inner Retinal Dysfunction in Diabetic Mice.Investigative ophthalmology & visual science · 2018Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes leads to dysfunction of the neural retina before and independent of classical microvascular diabetic retinopathy, but previous studies have failed to demonstrate which neurons and circuits are affected at the earliest stages. Here, using patch-clamp recording and two-photon Ca(2+) imaging in rat retinal slices, we investigated diabetes-evoked changes in a microcircuit consisting of rod bipolar cells and their dyad postsynaptic targets, AII and A17 amacrine cells, which play an essential role in processing scotopic visual signals. AII amacrines forward their signals to ON- and OFF-cone bipolar cells and A17 amacrines provide GABAergic feedback inhibition to rod bipolar cells. Whereas Ca(2+)-permeable AMPA receptors mediate input from rod bipolar cells to both AII and A17 amacrines, diabetes changes the synaptic receptors on A17, but not AII amacrine cells. This was expressed as a change in pharmacological properties and single-channel conductance of the synaptic receptors, consistent with an upregulation of the AMPA receptor GluA2 subunit and reduced Ca(2+) permeability. In addition, two-photon imaging revealed reduced agonist-evoked influx of Ca(2+) in dendritic varicosities of A17 amacrine cells from diabetic compared with normal animals. Because Ca(2+)-permeable receptors in A17 amacrine cells mediate synaptic release of GABA, the reduced Ca(2+) permeability of these receptors in diabetic animals leads to reduced release of GABA, followed by disinhibition and increased release of glutamate from rod bipolar cells. This perturbation of neuron and microcircuit dynamics can explain the decreased dynamic range and sensitivity of scotopic vision that has been observed in diabetes.
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