RGS7 and -11 complexes accelerate the ON-bipolar cell light response

Jianmei Zhang, Brett G. Jeffrey, Catherine Morgans, Neal S. Burke, Tammie L. Haley, Robert Duvoisin, R. Lane Brown

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Purpose. The retinal ON-bipolar cell (ON-BPC) light response is initiated upon deactivation of the metabotropic glutamate receptor mGluR6 and the G protein Go. G protein-based signaling cascades are typically accelerated by interaction of the G protein α subunit with a member of the regulator of G protein signaling (RGS) protein family. The goal of this study was to determine whether RGS7 and/or -11 serve this function in retinal ON-BPCs. Methods. Retinas from mice lacking RGS11 (RGS11-/-), or with a deletion mutation in RGS7 (RGS7Δ/Δ), or both, were compared to wild-type (WT) by immunofluorescence confocal microscopy. The retinal light response was measured with the electroretinogram (ERG). The kinetics of simulated light responses from individual rod bipolar cells were recorded by whole-cell patch-clamp electrophysiology. Results. Levels of the R7 RGS interaction partners, Gβ5 and R9AP, were reduced in the outer plexiform layer of the RGS11-/- and RGS7Δ/Δ/RGS11-/- mice. ERG recordings demonstrated a delay in the rising phase of the ERG b-wave, larger photopic b-wave amplitudes, and increased scotopic threshold response sensitivity in the RGS11-/- and RGS7Δ/Δ/RGS11-/- mice. The ERG measured from the RGS7Δ/Δ retina was normal. Patch-clamp recordings of chemically simulated light responses of rod BPCs revealed a 25-ms delay in the onset of the ON-BPC response in the RGS7Δ/Δ/RGS11-/- mouse compared with the WT. Conclusions. RGS11 plays a role in the deactivation of Gαo, which precedes activation of the depolarizing current in ONBPCs. RGS7 must also serve a role as changes in RGS7Δ/Δ/ RGS11-/- mice were greater than those in RGS11-/- mice.

Original languageEnglish (US)
Pages (from-to)1121-1129
Number of pages9
JournalInvestigative Ophthalmology and Visual Science
Volume51
Issue number2
DOIs
StatePublished - Feb 2010

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Light
GTP-Binding Proteins
Retina
Retinal Bipolar Cells
RGS Proteins
GTP-Binding Protein Regulators
Metabotropic Glutamate Receptors
Sequence Deletion
Electrophysiology
Protein Subunits
Fluorescence Microscopy
Confocal Microscopy

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience
  • Medicine(all)

Cite this

RGS7 and -11 complexes accelerate the ON-bipolar cell light response. / Zhang, Jianmei; Jeffrey, Brett G.; Morgans, Catherine; Burke, Neal S.; Haley, Tammie L.; Duvoisin, Robert; Lane Brown, R.

In: Investigative Ophthalmology and Visual Science, Vol. 51, No. 2, 02.2010, p. 1121-1129.

Research output: Contribution to journalArticle

Zhang, Jianmei ; Jeffrey, Brett G. ; Morgans, Catherine ; Burke, Neal S. ; Haley, Tammie L. ; Duvoisin, Robert ; Lane Brown, R. / RGS7 and -11 complexes accelerate the ON-bipolar cell light response. In: Investigative Ophthalmology and Visual Science. 2010 ; Vol. 51, No. 2. pp. 1121-1129.
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abstract = "Purpose. The retinal ON-bipolar cell (ON-BPC) light response is initiated upon deactivation of the metabotropic glutamate receptor mGluR6 and the G protein Go. G protein-based signaling cascades are typically accelerated by interaction of the G protein α subunit with a member of the regulator of G protein signaling (RGS) protein family. The goal of this study was to determine whether RGS7 and/or -11 serve this function in retinal ON-BPCs. Methods. Retinas from mice lacking RGS11 (RGS11-/-), or with a deletion mutation in RGS7 (RGS7Δ/Δ), or both, were compared to wild-type (WT) by immunofluorescence confocal microscopy. The retinal light response was measured with the electroretinogram (ERG). The kinetics of simulated light responses from individual rod bipolar cells were recorded by whole-cell patch-clamp electrophysiology. Results. Levels of the R7 RGS interaction partners, Gβ5 and R9AP, were reduced in the outer plexiform layer of the RGS11-/- and RGS7Δ/Δ/RGS11-/- mice. ERG recordings demonstrated a delay in the rising phase of the ERG b-wave, larger photopic b-wave amplitudes, and increased scotopic threshold response sensitivity in the RGS11-/- and RGS7Δ/Δ/RGS11-/- mice. The ERG measured from the RGS7Δ/Δ retina was normal. Patch-clamp recordings of chemically simulated light responses of rod BPCs revealed a 25-ms delay in the onset of the ON-BPC response in the RGS7Δ/Δ/RGS11-/- mouse compared with the WT. Conclusions. RGS11 plays a role in the deactivation of Gαo, which precedes activation of the depolarizing current in ONBPCs. RGS7 must also serve a role as changes in RGS7Δ/Δ/ RGS11-/- mice were greater than those in RGS11-/- mice.",
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T1 - RGS7 and -11 complexes accelerate the ON-bipolar cell light response

AU - Zhang, Jianmei

AU - Jeffrey, Brett G.

AU - Morgans, Catherine

AU - Burke, Neal S.

AU - Haley, Tammie L.

AU - Duvoisin, Robert

AU - Lane Brown, R.

PY - 2010/2

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N2 - Purpose. The retinal ON-bipolar cell (ON-BPC) light response is initiated upon deactivation of the metabotropic glutamate receptor mGluR6 and the G protein Go. G protein-based signaling cascades are typically accelerated by interaction of the G protein α subunit with a member of the regulator of G protein signaling (RGS) protein family. The goal of this study was to determine whether RGS7 and/or -11 serve this function in retinal ON-BPCs. Methods. Retinas from mice lacking RGS11 (RGS11-/-), or with a deletion mutation in RGS7 (RGS7Δ/Δ), or both, were compared to wild-type (WT) by immunofluorescence confocal microscopy. The retinal light response was measured with the electroretinogram (ERG). The kinetics of simulated light responses from individual rod bipolar cells were recorded by whole-cell patch-clamp electrophysiology. Results. Levels of the R7 RGS interaction partners, Gβ5 and R9AP, were reduced in the outer plexiform layer of the RGS11-/- and RGS7Δ/Δ/RGS11-/- mice. ERG recordings demonstrated a delay in the rising phase of the ERG b-wave, larger photopic b-wave amplitudes, and increased scotopic threshold response sensitivity in the RGS11-/- and RGS7Δ/Δ/RGS11-/- mice. The ERG measured from the RGS7Δ/Δ retina was normal. Patch-clamp recordings of chemically simulated light responses of rod BPCs revealed a 25-ms delay in the onset of the ON-BPC response in the RGS7Δ/Δ/RGS11-/- mouse compared with the WT. Conclusions. RGS11 plays a role in the deactivation of Gαo, which precedes activation of the depolarizing current in ONBPCs. RGS7 must also serve a role as changes in RGS7Δ/Δ/ RGS11-/- mice were greater than those in RGS11-/- mice.

AB - Purpose. The retinal ON-bipolar cell (ON-BPC) light response is initiated upon deactivation of the metabotropic glutamate receptor mGluR6 and the G protein Go. G protein-based signaling cascades are typically accelerated by interaction of the G protein α subunit with a member of the regulator of G protein signaling (RGS) protein family. The goal of this study was to determine whether RGS7 and/or -11 serve this function in retinal ON-BPCs. Methods. Retinas from mice lacking RGS11 (RGS11-/-), or with a deletion mutation in RGS7 (RGS7Δ/Δ), or both, were compared to wild-type (WT) by immunofluorescence confocal microscopy. The retinal light response was measured with the electroretinogram (ERG). The kinetics of simulated light responses from individual rod bipolar cells were recorded by whole-cell patch-clamp electrophysiology. Results. Levels of the R7 RGS interaction partners, Gβ5 and R9AP, were reduced in the outer plexiform layer of the RGS11-/- and RGS7Δ/Δ/RGS11-/- mice. ERG recordings demonstrated a delay in the rising phase of the ERG b-wave, larger photopic b-wave amplitudes, and increased scotopic threshold response sensitivity in the RGS11-/- and RGS7Δ/Δ/RGS11-/- mice. The ERG measured from the RGS7Δ/Δ retina was normal. Patch-clamp recordings of chemically simulated light responses of rod BPCs revealed a 25-ms delay in the onset of the ON-BPC response in the RGS7Δ/Δ/RGS11-/- mouse compared with the WT. Conclusions. RGS11 plays a role in the deactivation of Gαo, which precedes activation of the depolarizing current in ONBPCs. RGS7 must also serve a role as changes in RGS7Δ/Δ/ RGS11-/- mice were greater than those in RGS11-/- mice.

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