May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Compartmental Localization Of GABAB Receptors On Starburst Amacrine Cell Dendrites In The Rabbit Retina
Author Affiliations & Notes
  • C.L. Zucker
    Dept of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA
  • B. Ehinger
    Ophthalmology, University of Lund, Lund, Sweden
  • N.M. Grzywacz
    Department of Biomedical Engineering, University of Southern California, Los Angeles, CA
  • Footnotes
    Commercial Relationships  C.L. Zucker, None; B. Ehinger, None; N.M. Grzywacz, None.
  • Footnotes
    Support  NIH Grants EY07552 (CLZ), EY08921 & EY11170 (NMG), MFR project 2321 (BE).
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 5362. doi:https://doi.org/
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      C.L. Zucker, B. Ehinger, N.M. Grzywacz; Compartmental Localization Of GABAB Receptors On Starburst Amacrine Cell Dendrites In The Rabbit Retina . Invest. Ophthalmol. Vis. Sci. 2004;45(13):5362. doi: https://doi.org/.

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

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Abstract

Abstract: : Purpose: Starburst amacrine cells contain both acetylcholine and GABA, and are known to interact with ON–OFF directionally selective ganglion cells in such a way as to play prominently in the production of the physiological properties of these cells. Physiological and pharmacological data suggests that a glycinergic cholinoceptive amacrine cell type is involved in a GABAB mediated feedback loop with starburst amacrine cells that modifies the release of acetylcholine. We have shown that the so–called DAPI–3 cell is itself glycinergic and is cholinoceptive. In addition, we have also found that starburst amacrine cells, but not DAPI–3 cells, contain GABAB receptors. In order to reconcile our findings with the data of Neal & Cunningham (1995), we have proposed a model that suggests that the GABAB receptors would be localized to certain starburst amacrine cell dendritic compartments but not at others. Thus, in the present study, we have investigated the dendritic placement of GABAB receptors on starburst amacrine cells. Methods: We have used confocal analysis of intracellularly filled starburst amacrine cells double–labeled for GABAB receptors. Image stacks encompassing the entire extent of starburst amacrine cell dendrites and terminals were analyzed. Multi–axis channel rotations were statistically analyzed to determine the degree of double–labeling vs. random association. Results: Most GABAB receptors were found to be localized to varicosities along starburst amacrine cell dendrites. In total, 36% of starburst amacrine cell varicosities showed GABAB receptor immunoreactivity with the remaining varicosities being receptor negative. This pattern was consistent over the entire length of starburst amacrine cell dendrites with no proximal/distal differences seen. Conclusions: The GABAB receptor–localization pattern on starburst amacrine cells along with muscarinic–receptor localization on a bistratified glycinergic amacrine cell (DAPI–3 cell) suggest an anatomical construct that may underlie a circuit involved in cholinergic modulation of retinal function. The boutons that contain GABAB autoreceptors may serve as sites where GABA locally inhibits the release of acetylcholine to glycinergic cells. Disinhibition of the glycinergic feedback to the starburst cells may then facilitate release of acetylcholine from the other boutons. This facilitation is consistent with the findings of Neal and Cunningham (1995).

Keywords: amacrine cells • retina: proximal (bipolar, amacrine, and ganglion cells) • retinal connections, networks, circuitry 
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