May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Bipolar and Amacrine Inputs Modulating Ganglion–Cell Photoreceptors
Author Affiliations & Notes
  • K.Y. Wong
    Neuroscience, Brown University, Providence, RI
  • D.M. Berson
    Neuroscience, Brown University, Providence, RI
  • Footnotes
    Commercial Relationships  K.Y. Wong, None; D.M. Berson, None.
  • Footnotes
    Support  5 T32 MH19118; EY 12793
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 2332. doi:
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      K.Y. Wong, D.M. Berson; Bipolar and Amacrine Inputs Modulating Ganglion–Cell Photoreceptors . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2332.

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

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Abstract: : Purpose: To characterize excitatory and inhibitory synaptic inputs to intrinsically photosensitive retinal ganglion cells (ipRGCs) and their interaction with the endogenous photoresponse. Methods: We made whole–cell recordings of adult rat ipRGCs in superfused eyecups at 34 °C. ipRGCs were identified by retrolabeling from the suprachiasmatic nucleus, sluggish light response kinetics, and persistent photosensitivity under synaptic blockade. Agonists were puffed in the presence of cobalt to ensure direct action of the drugs on ipRGCs. Antagonists were bath applied under conditions permitting synaptic transmission. Results: All ipRGCs responded to GABA, glycine and kainate, and some also to NMDA, indicating the presence of inhibitory and excitatory receptors. Direct inhibitory synaptic input (presumably from amacrine cells) was detectable at rest, since GABA and glycine antagonists reduced synaptic noise when ipRGCs were voltage–clamped at the cationic reversal potential. Most ipRGCs also received direct excitatory input (presumably from bipolar cells), as light evoked fast, mostly transient, synaptically mediated responses in the presence of GABA and glycine antagonists. These responses occurred at light ON or at both ON and OFF, and the ON depolarizations were blocked selectively when L–AP4 was applied in addition to the GABA and glycine antagonists. Thus, some cells had direct input from ON but not OFF bipolar cells whereas others were contacted by both ON and OFF bipolars. When most inhibitory and excitatory inputs were blocked with bicuculline, TPMPA, strychnine, L–AP4, D–AP5 and DNQX, the intrinsic response of ipRGCs increased in amplitude, typically by about 50%. Conclusions: Light affects the great majority of ipRGCs not only by triggering their intrinsic phototransduction but also through direct glutamatergic synaptic inputs from ON and OFF bipolar cells and through GABAergic and glycinergic amacrine cell contacts. These synaptic inputs, which are far more prevalent than previously recognized in rodent ipRGCs, serve in part to attenuate the intrinsic light response. Thus, the gain of ipRGC light responses is regulated by synaptic networks as well as by adaptation of the phototransduction cascade (see Wong et al., SfN 2004). These inputs to ipRGCs also provide a route through which the rods and cones can regulate a variety of non–image forming visual behaviors such as resetting the master circadian clock.

Keywords: retina: proximal (bipolar, amacrine, and ganglion cells) • ganglion cells • circadian rhythms 

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