May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Light and Dopamine Modulate the Sodium Channel Activity in Transient ON Bipolar Cells
Author Affiliations & Notes
  • T. Ichinose
    Ophthalmology, Washington Univ Sch Med, St Louis, MO
  • P.D. Lukasiewicz
    Ophthalmology, Washington Univ Sch Med, St Louis, MO
  • Footnotes
    Commercial Relationships  T. Ichinose, None; P.D. Lukasiewicz, None.
  • Footnotes
    Support  EY08922, EY02687, Research to Prevent Blindness, The M. Bauer Foundation
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 609. doi:
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      T. Ichinose, P.D. Lukasiewicz; Light and Dopamine Modulate the Sodium Channel Activity in Transient ON Bipolar Cells . Invest. Ophthalmol. Vis. Sci. 2005;46(13):609.

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

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Abstract: : Purpose: We have shown previously that sustained voltage–gated sodium currents are observed in transient ON bipolar cells whose axon terminals ramify in the mid–IPL, and that these currents enhance visual information in the transient bipolar cell–ganglion cell pathway. To determine the effect of light adaptation on this signaling pathway, we have examined the sodium current in transient ON bipolar cells and its effect on signaling to ganglion cells in dark– and light–adapted retinas. Methods: Whole cell recordings were made from transient bipolar and ganglion cells in salamander retinal slices. Sodium currents were recorded from transient ON bipolar cells in dark– and light–adapted retinas. Transient light–evoked excitatory postsynaptic currents (L–EPSCs) were recorded at light onset from ganglion cells. L–EPSCs were recorded with dim, then bright background illumination in a single ganglion cell. Results: In transient ON bipolar cells with axon terminals ramifying in the mid–IPL, inward sodium currents were observed in response to positive voltage steps after responses measured in the presence of tetrodotoxin (TTX), a sodium channel blocker, were subtracted from control responses. In dark adapted retinas the sodium currents were prolonged (time constant (τ) =87.0 ± 29 msec) with peak amplitudes of –96.7 ± 12 pA (n=6). Surprisingly, sodium currents in light adapted retinas were more transient (τ =3.6 ± 1.9 msec, n=5) and had smaller amplitudes (–37.1 ± 11 pA). A dopamine receptor agonist, ADTN (50 µM) mimicked light adaptation. ADTN reduced the sodium currents in dark adapted retinas (peak= –38.4 ± 12 pA, τ =6.6 ± 3.4 msec, n=5). We examined whether the bipolar cell sodium currents affected light responses in ganglion cells differently in dark– and light–adapted retinas. In dark–adapted retinas, TTX reduced the L–EPSCs by 68.6 ± 11 % (n=7). However, when the same preparation was light–adapted, TTX reduced L–EPSCs only by 32.9 ± 13 % (p<0.01 vs. dark adapted retina). In dark adapted retinas ADTN reduced L–EPSCs in transient ganglion cells (48.1 ± 4.7 %, n=4), and occluded the TTX effect. Conclusions: We found that TTX sensitive sodium currents in transient ON bipolar cells were larger in dark–adapted retinas than in light–adapted retinas. The bipolar cell sodium currents amplify light evoked inputs to ganglion cells more under dark–adapted compared to light–adapted conditions. The modulatory effect of light was mimicked by a dopamine agonist. This may represent a novel mechanism of light adaptation for temporal visual signaling.

Keywords: electrophysiology: non-clinical • retina: proximal (bipolar, amacrine, and ganglion cells) • ion channels 

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