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Pharmacological analysis of intrinsic neuronal oscillations in rd10 retina.

In the widely used mouse model of retinal degeneration, rd1, the loss of photoreceptors leads to rhythmic electrical activity of around 10–16 Hz in the remaining retinal network. Recent studies suggest that this oscillation is formed within the electrically coupled network of AII amacrine cells and... Full description

Journal Title: PloS one 2014, Vol.9(6), p.e99075
Main Author: Biswas, Sonia
Other Authors: Haselier, Christine , Mataruga, Anja , Thumann, Gabriele , Walter, Peter , Müller, Frank
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; DOI: 1932-6203 ; DOI: 10.1371/journal.pone.0099075
Link: http://search.proquest.com/docview/1535622705/?pq-origsite=primo
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title: Pharmacological analysis of intrinsic neuronal oscillations in rd10 retina.
format: Article
creator:
  • Biswas, Sonia
  • Haselier, Christine
  • Mataruga, Anja
  • Thumann, Gabriele
  • Walter, Peter
  • Müller, Frank
subjects:
  • Animals–Drug Effects
  • Mice–Cytology
  • Neurons–Drug Effects
  • Retina–Physiology
ispartof: PloS one, 2014, Vol.9(6), p.e99075
description: In the widely used mouse model of retinal degeneration, rd1, the loss of photoreceptors leads to rhythmic electrical activity of around 10–16 Hz in the remaining retinal network. Recent studies suggest that this oscillation is formed within the electrically coupled network of AII amacrine cells and ON-bipolar cells. A second mouse model, rd10 , displays a delayed onset and slower progression of degeneration, making this mouse strain a better model for human retinitis pigmentosa. In rd10 , oscillations occur at a frequency of 3–7 Hz, raising the question whether oscillations have the same origin in the two mouse models. As rd10 is increasingly being used as a model to develop experimental therapies, it is important to understand the mechanisms underlying the spontaneous rhythmic activity. To study the properties of oscillations in rd10 retina we combined multi electrode recordings with pharmacological manipulation of the retinal network. Oscillations were abolished by blockers for ionotropic glutamate receptors and gap junctions. Frequency and amplitude of oscillations were modulated strongly by blockers of inhibitory receptors and to a lesser extent by blockers of HCN channels. In summary, although we found certain differences in the pharmacological modulation of rhythmic activity in rd10 compared to rd1 , the overall pattern looked similar. This suggests that the generation of rhythmic activity may underlie similar mechanisms in rd1 and rd10 retina.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 1932-6203 ; DOI: 10.1371/journal.pone.0099075
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titlePharmacological analysis of intrinsic neuronal oscillations in rd10 retina.
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descriptionIn the widely used mouse model of retinal degeneration, rd1, the loss of photoreceptors leads to rhythmic electrical activity of around 10–16 Hz in the remaining retinal network. Recent studies suggest that this oscillation is formed within the electrically coupled network of AII amacrine cells and ON-bipolar cells. A second mouse model, rd10 , displays a delayed onset and slower progression of degeneration, making this mouse strain a better model for human retinitis pigmentosa. In rd10 , oscillations occur at a frequency of 3–7 Hz, raising the question whether oscillations have the same origin in the two mouse models. As rd10 is increasingly being used as a model to develop experimental therapies, it is important to understand the mechanisms underlying the spontaneous rhythmic activity. To study the properties of oscillations in rd10 retina we combined multi electrode recordings with pharmacological manipulation of the retinal network. Oscillations were abolished by blockers for ionotropic glutamate receptors and gap junctions. Frequency and amplitude of oscillations were modulated strongly by blockers of inhibitory receptors and to a lesser extent by blockers of HCN channels. In summary, although we found certain differences in the pharmacological modulation of rhythmic activity in rd10 compared to rd1 , the overall pattern looked similar. This suggests that the generation of rhythmic activity may underlie similar mechanisms in rd1 and rd10 retina.
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