June 2015
Volume 56, Issue 7
ARVO Annual Meeting Abstract  |   June 2015
Cell-autonomous changes in displaced cholinergic amacrine cells lacking Gβ5
Author Affiliations & Notes
  • Ching-Kang Jason Chen
    Ophthalmology, Baylor College of Medicine, Houston, TX
    Biochemistry and Molecular Biology, Baylor College of Medicine, Houston, TX
  • April Bang
    Ophthalmology, Baylor College of Medicine, Houston, TX
  • Yu-Jiun Chen
    Ophthalmology, Baylor College of Medicine, Houston, TX
  • Adam Rory McQuiston
    Anatomy and Neurobiology, Virginia Commonwealth University, Richmond, VA
  • Hung-Ya Tu
    Ophthalmology, Baylor College of Medicine, Houston, TX
  • Chuan-Chin Chiao
    Life Science, National Tsing Hua University, Hsinchu, Taiwan
    Systems Neuroscience, National Tsing Hua University, Hsinchu, Taiwan
  • Footnotes
    Commercial Relationships Ching-Kang Chen, None; April Bang, None; Yu-Jiun Chen, None; Adam McQuiston, None; Hung-Ya Tu, None; Chuan-Chin Chiao, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 3231. doi:
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      Ching-Kang Jason Chen, April Bang, Yu-Jiun Chen, Adam Rory McQuiston, Hung-Ya Tu, Chuan-Chin Chiao; Cell-autonomous changes in displaced cholinergic amacrine cells lacking Gβ5. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):3231.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: Mice lacking the fifth and unconventional beta subunit of heterotrimeric G-proteins (Gβ5), which is the obligate partner of R7 subfamily of Regulators of G-protein Signaling (RGS) proteins, have abnormal dendritic morphology in retinal ON-bipolar cells. We hereby investigate whether similar changes are present in additional retinal neurons and whether such changes occur via a cell-autonomous mechanism.

Methods: We sought to conditionally inactivate Gβ5 in cholinergic neurons by first floxing a 2.7kb XhoI fragment harboring the third exon. The resulting Gβ5floxed/floxed (Gβ5F/F) mouse was then mated into a commercial cholinergic Cre driver background (Jax stock #: 006410). To label cholinergic neurons for recording, the Ai9 reporter background (Jax stock #: 007909) was then introduced into both cholinergic-specific Gβ5 knockout and straight Gβ5 knockout backgrounds. Patch clamp recordings in the current clamp mode were used to examine changes in membrane potentials while filling cells with biocytin. Morphology of recorded cells was recovered by Streptavidin-Alexa488 staining, confocally imaged, and traced in Neurolucida for morphometric analysis.

Results: Nearly all of the so-called starburst cholinergic amacrine cells (SAC) can be genetically marked. We found in straight Gβ5 knockout mice that membrane potentials of displaced SACs in the ganglion cell layer underwent rhythmic fluctuations with characteristic frequencies and amplitudes under our experimental conditions. Such rhythmic changes were not apparent in cholinergic-specific conditional Gβ5 knockout mice. Dendritic area and total dendrite length of displaced SACs, however, decreased significantly in both straight and conditional Gβ5-/- knockout mice when compared to those from control animals.

Conclusions: These data suggest that the loss of Gβ5 in displaced SACs causes cell-autonomous changes in dendritic morphology and that rhythmic fluctuation in SAC membrane potential is independent of the observed morphological changes. We speculate that membrane potential fluctuation may be secondary to the loss of normal synaptic transmission between photoreceptors and ON-bipolar cells in straight Gβ5 knockout mice.


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