September 2016
Volume 57, Issue 12
Open Access
ARVO Annual Meeting Abstract  |   September 2016
Spiking and non-spiking mechanisms control ganglion cell excitatory input at different contrasts and temporal frequencies
Author Affiliations & Notes
  • Ben Murphy-Baum
    Casey Eye Institute, Dept. of Ophthalmology, Oregon Health and Science University, Portland, Oregon, United States
  • William Rowland Taylor
    Casey Eye Institute, Dept. of Ophthalmology, Oregon Health and Science University, Portland, Oregon, United States
  • Footnotes
    Commercial Relationships   Ben Murphy-Baum, None; William Taylor, None
  • Footnotes
    Support  RO1 EY014888, T32 EY023211, P30 EY010572, P30 NS061800, and unrestricted funding from Research to Prevent Blindness
Investigative Ophthalmology & Visual Science September 2016, Vol.57, No Pagination Specified. doi:
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      Ben Murphy-Baum, William Rowland Taylor; Spiking and non-spiking mechanisms control ganglion cell excitatory input at different contrasts and temporal frequencies. Invest. Ophthalmol. Vis. Sci. 201657(12):.

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

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Abstract

Purpose : The excitatory input to retinal ganglion cells (RGCs) can be regulated by mechanisms both within and outside of the center receptive field (RF). Outside the center RF, action potentials are thought to drive long-range GABAergic feedback onto bipolar cell terminals, whereas feedback triggered from within the center RF can often function without spiking activity. NaV channel activity or spikes in bipolar cells may also affect RGC excitatory input. We asked whether spike-dependent (SD) and spike-independent (SI) mechanisms have different roles in regulating the excitatory input to RGCs under various visual conditions.

Methods : Excitatory postsynaptic currents (EPSCs) were recorded from OFF alpha ganglion cells in whole-mount rabbit retinas in response to visual stimuli that varied in size, contrast, and temporal frequency. TTX (200 nM) was applied to block SD mechanisms, while SR-95531 (10 µM, GABAA antagonist) and TPMPA (100 µM, GABAC antagonist) were subsequently added to block SI mechanisms that relied on GABAergic signaling.

Results : At low temporal frequencies, blocking SD mechanisms potentiated EPSC amplitudes at high contrast (617 ± 67 to 811 ± 81 pA at 1 Hz, 80% contrast), whereas blocking SI mechanisms potentiated them at low contrast (245 ± 16 to 486 ± 66 pA at 1 Hz, 5% contrast). At high temporal frequencies, blocking SD mechanisms had the opposite affect, suppressing EPSC amplitudes from 676 ± 85 to 220 ± 51 pA (14.1 Hz, 80% contrast). Blocking either mechanism also shifted the EPSC phase later in the stimulus cycle. Similar to the amplitude modulation, blocking SD mechanisms dominated the phase delay at high contrast (1.3 ± 0.2 rad at 10 Hz, 80% contrast), whereas SI mechanisms dominated at low contrast (1.4 ± 0.26 rad at 10 Hz, 2% contrast).

Conclusions : The data indicate that NaV activity, likely within bipolar cells, boosts RGC excitatory input during high contrast and high frequency stimulation. At low contrast and low frequencies SI GABAergic inhibition suppressed EPSCs, independent of NaV activity, possibly via local inhibitory feedback circuits. Increasing contrast at low temporal frequencies activated SD suppression of EPSCs, suggesting increased spiking activity in wide-field amacrine cells. Overall, NaV activity and inhibition act synergistically to tune OFF alpha ganglion cells to higher temporal frequencies and faster response times.

This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.

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