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Postsynaptic Plasticity Triggered by Ca.sup.2+-Permeable AMPA Receptor Activation in Retinal Amacrine Cells

Byline: Mean-Hwan Kim, Henrique von Gersdorff 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 b... Full description

Journal Title: Neuron (Cambridge Mass.), 2016-02-03, Vol.89 (3), p.507
Main Author: Kim, Mean-Hwan
Other Authors: Von Gersdorff, Henrique
Format: Electronic Article Electronic Article
Language: English
Subjects:
Glutamate
Ophthalmology
Physiological aspects
Quelle: Alma/SFX Local Collection
Publisher: Elsevier B.V
ID: ISSN: 0896-6273
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title: Postsynaptic Plasticity Triggered by Ca.sup.2+-Permeable AMPA Receptor Activation in Retinal Amacrine Cells
format: Article
creator:
  • Kim, Mean-Hwan
  • Von Gersdorff, Henrique
subjects:
  • Glutamate
  • Ophthalmology
  • Physiological aspects
ispartof: Neuron (Cambridge, Mass.), 2016-02-03, Vol.89 (3), p.507
description: Byline: Mean-Hwan Kim, Henrique von Gersdorff 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 [Ca.sup.2+].sub.i rises. However, strong postsynaptic Ca.sup.2+ buffering with BAPTA abolished the potentiation and selective antagonists of Ca.sup.2+-permeable AMPA receptors also blocked the potentiation of AMPA-mediated currents. Together these results suggest that Ca.sup.2+ influx via Ca.sup.2+-permeable AMPA receptors can elicit a rapid form of postsynaptic plasticity in a subgroup of amacrine cell dendrites. Author Affiliation: (1) The Vollum Institute, Oregon Health & Science University, Portland, OR 97239, USA (2) Department of Ophthalmology, Casey Eye Institute, Oregon Health & Science University, Portland, OR 97239, USA (3) Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR 97239, USA Article History: Received 12 June 2015; Revised 18 July 2015; Accepted 15 December 2015 Article Note: (miscellaneous) Published: January 21, 2016
language: eng
source: Alma/SFX Local Collection
identifier: ISSN: 0896-6273
fulltext: fulltext
issn:
  • 0896-6273
  • 1097-4199
url: Link


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titlePostsynaptic Plasticity Triggered by Ca.sup.2+-Permeable AMPA Receptor Activation in Retinal Amacrine Cells
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descriptionByline: Mean-Hwan Kim, Henrique von Gersdorff 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 [Ca.sup.2+].sub.i rises. However, strong postsynaptic Ca.sup.2+ buffering with BAPTA abolished the potentiation and selective antagonists of Ca.sup.2+-permeable AMPA receptors also blocked the potentiation of AMPA-mediated currents. Together these results suggest that Ca.sup.2+ influx via Ca.sup.2+-permeable AMPA receptors can elicit a rapid form of postsynaptic plasticity in a subgroup of amacrine cell dendrites. Author Affiliation: (1) The Vollum Institute, Oregon Health & Science University, Portland, OR 97239, USA (2) Department of Ophthalmology, Casey Eye Institute, Oregon Health & Science University, Portland, OR 97239, USA (3) Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR 97239, USA Article History: Received 12 June 2015; Revised 18 July 2015; Accepted 15 December 2015 Article Note: (miscellaneous) Published: January 21, 2016
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issn0896-6273
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abstractByline: Mean-Hwan Kim, Henrique von Gersdorff 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 [Ca.sup.2+].sub.i rises. However, strong postsynaptic Ca.sup.2+ buffering with BAPTA abolished the potentiation and selective antagonists of Ca.sup.2+-permeable AMPA receptors also blocked the potentiation of AMPA-mediated currents. Together these results suggest that Ca.sup.2+ influx via Ca.sup.2+-permeable AMPA receptors can elicit a rapid form of postsynaptic plasticity in a subgroup of amacrine cell dendrites. Author Affiliation: (1) The Vollum Institute, Oregon Health & Science University, Portland, OR 97239, USA (2) Department of Ophthalmology, Casey Eye Institute, Oregon Health & Science University, Portland, OR 97239, USA (3) Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR 97239, USA Article History: Received 12 June 2015; Revised 18 July 2015; Accepted 15 December 2015 Article Note: (miscellaneous) Published: January 21, 2016
pubElsevier B.V
doi10.1016/j.neuron.2015.12.028