Abstract
An essential feature of the first synapse in the retina is a negative feedback pathway from horizontal cells to cones. Here we show that at this synapse, connexin26 forms hemichannels on horizontal cell dendrites near the glutamate release site of the cones. Blocking these hemichannels hyperpolarizes horizontal cells, modulates the Ca2+ channels of the cones, and abolishes all feedback-mediated responses. We propose a feedback mechanism in which the activity of the Ca2+ channels and the subsequent glutamate release of the cones are modulated by a current through these hemichannels. Because the current through the hemichannels depends on the polarization of the horizontal cells, their activity modulates the output of the cones.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcium / metabolism
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Calcium Channels / metabolism
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Carbenoxolone / pharmacology
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Carps / physiology*
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Connexin 26
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Connexins / antagonists & inhibitors
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Connexins / chemistry
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Connexins / metabolism*
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Dendrites / drug effects
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Dendrites / metabolism
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Electric Conductivity
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Excitatory Amino Acid Agonists / pharmacology
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Feedback
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Glutamic Acid / metabolism
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Glutamic Acid / pharmacology
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Immunohistochemistry
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Ion Channel Gating / drug effects
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Kainic Acid / pharmacology
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Light
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Membrane Potentials / drug effects
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Models, Neurological
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Retina / cytology
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Retina / drug effects
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Retina / metabolism*
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Retinal Cone Photoreceptor Cells / cytology
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Retinal Cone Photoreceptor Cells / drug effects
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Retinal Cone Photoreceptor Cells / metabolism
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Synapses / drug effects
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Synapses / metabolism
Substances
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Calcium Channels
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Connexins
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Excitatory Amino Acid Agonists
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Connexin 26
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Glutamic Acid
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Carbenoxolone
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Kainic Acid
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Calcium