April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Paired Recordings Of Dopaminergic Amacrines And ipRGCs
Author Affiliations & Notes
  • Matthew J. Van Hook
    Department of Neuroscience, Brown University, Providence, Rhode Island
  • David M. Berson
    Department of Neuroscience, Brown University, Providence, Rhode Island
  • Footnotes
    Commercial Relationships  Matthew J. Van Hook, None; David M. Berson, None
  • Footnotes
    Support  NIH Grants R01 EY 12793, R01 EY 17137, and 1 T32 NS062443-01
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4553. doi:
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      Matthew J. Van Hook, David M. Berson; Paired Recordings Of Dopaminergic Amacrines And ipRGCs. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4553.

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

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Purpose: : Intrinsically photosensitive retinal ganglion cells (ipRGCs) blend inhibitory and excitatory synaptic influences, with direct, melanopsin-based photoresponses. The resulting output signals feed non-image forming visual centers of the brain, and appear to influence the retina itself. Prior evidence suggests that M1-type ipRGCs interact bidirectionally with dopaminergic amacrine cells (DACs). Here, we asked whether DACs, which are thought to co-release GABA, are a source of GABAergic input onto ipRGCs and sought direct evidence for an ipRGC-to-DAC excitatory synapse.

Methods: : To explore possible synaptic interactions between ipRGCs and DACs, we made paired whole-cell recordings in flat-mounted mouse retina from M1-type ipRGCs and DACs, which costratify in the outermost IPL. In order to target cells for recording, we interbred two existing mouse lines (TH::RFP and Opn4cre/+;Z/EG) so that the two cell types were labeled with distinct fluorophores. To test for synaptic interactions, we depolarized the presumptive presynaptic cell while voltage-clamping the postsynaptic cell to isolate excitatory or inhibitory post-synaptic currents.

Results: : We recorded from 19 M1 ipRGCs and DAC pairs. When ipRGCs were voltage-clamped at the cationic reversal potential, they typically exhibited spontaneous inhibitory post-synaptic currents (IPSCs). Depolarizing the DAC with either a step (n = 13 pairs) or using previously-recorded action potentials as a voltage-clamp command (n = 5 pairs) failed to evoke additional, time-locked IPSCs in the ipRGC. Likewise, we did not detect evoked post-synaptic currents when we used a high chloride concentration in the ipRGC recording pipette and voltage-clamped the cell to increase the Cl- driving force (n = 3). In one pair, step depolarization of the ipRGC evoked a train of excitatory post-synaptic currents (EPSCs) in a DAC that were blocked by the ionotropic glutamate receptor antagonist DNQX.

Conclusions: : Although several pieces of evidence suggest that DACs are likely the source of GABA input onto M1-type ipRGCs, we were unable to evoke IPSCs in ipRGCs by stimulating DACs. This raises the possibility that DACs are not the source of GABA input. The presence of a glutamatergic synapse from ipRGCs to DACs is consistent with published reports.

Keywords: ganglion cells • amacrine cells • synapse 

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