May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Glycine Receptors and Glycinergic Synaptic Input at the Axon Terminals of Mammalian Retinal Rod Bipolar Cells
Author Affiliations & Notes
  • J. Cui
    Anatomy/Cell Biology, Wayne State Univ, Detroit, MI, United States
  • Y. Ma
    Anatomy/Cell Biology, Wayne State Univ, Detroit, MI, United States
  • S.A. Lipton
    Center for Neuroscience & Aging, Burnham Institute, La Jolla, CA, United States
  • Z. Pan
    Center for Neuroscience & Aging, Burnham Institute, La Jolla, CA, United States
  • Footnotes
    Commercial Relationships  J. Cui, None; Y. Ma, None; S.A. Lipton, None; Z. Pan, None.
  • Footnotes
    Support  NIH RO1EY12180 (Pan), RO1EY05477 (Lipton), Vision Core Grant EY04068
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2071. doi:
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      J. Cui, Y. Ma, S.A. Lipton, Z. Pan; Glycine Receptors and Glycinergic Synaptic Input at the Axon Terminals of Mammalian Retinal Rod Bipolar Cells . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2071.

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

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Abstract

Abstract: : Purpose: Glycine is one of the major inhibitory neurotransmitters in the retina. In this study, we investigated the properties of glycine receptors and glycinergic synaptic inputs at the axon terminals of mammalian rod bipolar cells (RBCs). Methods:Whole-cell patch-clamp recordings were performed in isolated axon terminal and retinal slice preparations from the rat. Intracellular Ca2+ transients were monitored by Ca2+ imaging recordings. Results: Glycine current density at terminal endings was found to be more than one order of magnitude higher than that in the somatic/dendritic region. On the other hand, glycine currents in both the terminal and somatic/dendritic regions manifested similar sensitivity to picrotoxinin. Single channel activities recorded from terminals and somata displayed a similar main-state conductance (~46 pS). Application of glycine was found to effectively suppress K+-evoked intracellular Ca2+ increases at the terminals. Furthermore, in the presence of GABAA and GABAC antagonists, strychnine-sensitive chloride currents were evoked in RBCs by puffing kainate onto the inner plexiform layer of retinal slices. No such currents were observed in RBCs lacking axon terminals or if Ca2+ was replaced by Co2+ in the extracellular solution. Glycinergic synaptic currents also displayed discrete miniature events, which were partially blocked by TTX. Conclusions: Glycine receptors are highly concentrated at the axon terminals of RBCs. The pharmacological and physiological properties of glycine receptors located at axon terminals and at somatic/dendritic regions appear to be the same. This study provides evidence for the existence of functional glycinergic synaptic input at RBC axon terminals that may play a role in modulating their synaptic transmission.

Keywords: inhibitory receptors • retina: proximal(bipolar, amacrine, and gangli • bipolar cells 
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