May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Glycinergic Mediated Response In Rod Bipolar Cells Of The rd Mouse
Author Affiliations & Notes
  • P. De la Villa
    Physiology, Univ of Alcala, Madrid, Spain
  • R. Barhoum
    Physiology, Univ of Alcala, Madrid, Spain
  • N. Forns
    Physiology, Univ of Alcala, Madrid, Spain
  • F. Germain
    Physiology, Univ of Alcala, Madrid, Spain
  • E.J. De la Rosa
    Developmental Neuroscience, CIB–CSIC, Madrid, Spain
  • Footnotes
    Commercial Relationships  P. De la Villa, None; R. Barhoum, None; N. Forns, None; F. Germain, None; E.J. De la Rosa, None.
  • Footnotes
    Support  SAF01–1038–C02
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 5074. doi:
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      P. De la Villa, R. Barhoum, N. Forns, F. Germain, E.J. De la Rosa; Glycinergic Mediated Response In Rod Bipolar Cells Of The rd Mouse . Invest. Ophthalmol. Vis. Sci. 2004;45(13):5074.

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

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Abstract

Abstract: : Purpose: In the present work we have studied the glycine induced currents at the axon terminal of rod bipolar cells (RBCs) from the rd mouse retina. The rd mice have been widely used as animal models of Retinitis Pigmentosa. Morphological and functional modifications at the level of the outer plexiform layer have been shown (Strettoi & Pignatelli, PNAS, 97:11020, 2000, Varela et al., Vision Res., 23: 312, 2003). Structural modifications at the level of the inner plexiform layer have also been shown (Strettoi et al., J.Neurosci. 22: 5492, 2002), consisting in dramatic structural changes suffered by rod bipolar cells axon terminals. However, very little is known about the functional changes suffered by these cells at the axon terminals. Methods: Currents induced by glycine were studied by the patch clamp technique in the whole cell configuration, on RBCs acutely dissociated from the rd mouse retina. Data from animals with retinal degeneration were compared with those from non–degenerated retina. Glycine (30 – 100 µM) were applied from a puff pipette in the near proximity of cell axon terminal and their evoked currents studied in RBCs clamped at membrane potentials (Vh=–40 mV). Results: In RBCs from dystrophic and non–dystrophic mouse retina, puff application of glycine induces chloride–mediated currents. The glycine–induced current was apparently larger in RBCs of the rd mouse. Dose–response curves were analyzed in the retinas of control and dystrophic animals. The mean amplitude of currents induced by glycine application in RBCs from rd animals were larger that those observed in non–degenerated animals. At saturating concentrations, glycine induced currents of ca. 300 pA were observed in RBC of control animals clamped at –40 mV. Glycine induced currents of ca. 500 pA were recorded from RBCs of dystrophic animals in similar experimental conditions. Current/voltage relationship of the glycine induced currents were also measured in RBCs from dystrophic and non dystrophic animals. A two fold increase in the glycine mediated conductance was observed in RBCs from dystrophic animals. Conclusions: In addition to the dendrite modifications in RBCs of the rd mouse, after the degeneration of rod photoreceptors, RBCs experience significant functional changes at the axon terminal. This work describes the functional changes that affect RBCs at the IPL level after photoreceptor degeneration

Keywords: bipolar cells • retinal degenerations: cell biology • neurotransmitters/neurotransmitter systems 
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