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Simultaneous Whole-cell Recordings from Photoreceptors and Second-order Neurons in an Amphibian Retinal Slice Preparation
Published on: June 1, 2013
RGS7 and -11 complexes accelerate the ON-bipolar cell light response
Jianmei Zhang1, Brett G Jeffrey, Catherine W Morgans
1Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman, Washington, USA.
Investigative Ophthalmology & Visual Science
|October 3, 2009
Summary
Regulator of G protein signaling 11 (RGS11) is crucial for deactivating G protein Go in retinal ON-bipolar cells. Loss of RGS11, and to a lesser extent RGS7, delays visual signaling and alters retinal light responses.
Area of Science:
- Neuroscience
- Cell Biology
- Vision Science
Background:
- The light response in retinal ON-bipolar cells (ON-BPCs) begins with the deactivation of the metabotropic glutamate receptor mGluR6 and the G protein Go.
- Regulator of G protein signaling (RGS) proteins typically accelerate G protein signaling cascades by interacting with the G protein alpha subunit.
Purpose of the Study:
- To investigate the role of RGS7 and RGS11 in the function of retinal ON-BPCs.
- To determine if RGS7 and/or RGS11 accelerate the deactivation of the G protein Go in ON-BPCs.
Main Methods:
- Immunofluorescence confocal microscopy was used to compare retinas from wild-type (WT) mice with those lacking RGS11 (RGS11(-/-)), RGS7 (RGS7(Delta/Delta)), or both.
- Electroretinogram (ERG) was employed to measure the overall retinal light response.
- Whole-cell patch-clamp electrophysiology recorded the kinetics of simulated light responses from individual rod bipolar cells.
Main Results:
- Reduced levels of RGS7 RGS interaction partners (Gbeta5 and R9AP) were observed in the outer plexiform layer of RGS11(-/-) and RGS7(Delta/Delta)/RGS11(-/-) mice.
- ERG recordings in RGS11(-/-) and RGS7(Delta/Delta)/RGS11(-/-) mice showed delayed b-wave rising phases, larger photopic b-wave amplitudes, and increased scotopic threshold response sensitivity.
- Patch-clamp recordings revealed a 25-ms delay in the onset of the ON-BPC response in RGS7(Delta/Delta)/RGS11(-/-) mice compared to WT, while RGS7(Delta/Delta) mice showed normal ERG.
- The ERG of RGS7(Delta/Delta) mice was normal, indicating RGS11 is the primary player.
Conclusions:
- RGS11 is essential for the deactivation of Galphao, a critical step preceding the activation of the depolarizing current in ON-BPCs.
- RGS7 also contributes to this process, as evidenced by more pronounced changes in mice lacking both RGS7 and RGS11 compared to those lacking only RGS11.
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