It has been reported previously using whole-cell patch recording of ipRGCs in the rat retina maintained in vitro, that L-AP4 abolishes ON depolarization in ipRGCs [10].
In ipRGCs, however, neither of the Ih blockers tested affected the membrane potential, suggesting that Ih is not active in ipRGCs at rest.
Unlike in other systems, however, Ih in ipRGCs apparently does not actively contribute to resting membrane potential.
However, analyses of the receptive field for synaptically mediated depolarizations in ipRGCs resembles that of the dendritic field of these cells suggesting that ipRGCs receive cone ON-bipolar inputs throughout their entire dendritic fields [10].
In ipRGCs, however, both the intrinsic and synaptically-driven light responses are exclusively depolarizing under physiological conditions and therefore do not bring the ipRGC membrane potential near the Ih activation threshold [1], [20].
Our study was not suited to explore such a contribution in ipRGCs because their dendrites were lost during cellular dissociation.
To examine the reversal potential and ion selectivity of Ih in ipRGCs, we performed a tail-current analysis (Fig. 4).
Thus, dopaminergic influences on Ih could provide a basis for light adaptation and circadian modulation of ipRGCs and of the non-image-forming visual mechanisms they support [30], [71], [72].
As in other systems, including other retinal ganglion cells, Ih in ipRGCs is characterized by slow kinetics and a slightly greater permeability for K+ than for Na+.
As elsewhere, Ih in ipRGCs reverses near −40 mV and is a mixed cation current with a moderate preference for K+ over Na+ [27].
