Intraretinal Aaxon Collaterals of Melanopsin Cells in Primate and Mouse Suggest a Novel Synaptic Pathway for Feedback of Irradiance Information to the Retina

摘要

The axons of retinal ganglion cells are unique in that they typically do not provide synaptic feedback to the retina via recurrent axon collaterals. Such collaterals, however, have been rarely but consistently observed in many species, including primate. The ganglion cells bearing these collaterals have large, sparsely branching dendritic trees, suggesting the collaterals are not a developmental aberration but are associated with a single, low-density ganglion cell type. Here we show that, in both mouse and primate, intraretinal collaterals arise from a subset of melanopsin-expressing cells, suggesting a critical role for this novel feedback pathway in retinal circadian rhythms. Using a transgenic mouse (Opn4 CreERT2; Z/AP) in which the density of labeled melanopsin cells is controlled by tamoxifen injection, we show axon collaterals that terminate in either the inner or outer IPL and can be clearly traced to individual melanopsin cell primary axons (a??8% of cells). In macaque retina, a subpopulation (a??11%) of melanopsin immunoreactive cells also exhibit axon collaterals. It has been shown that dopaminergic amacrine cells, a modulator in retinal circadian rhythms, also show a melanopsin driven light response (Zhang et al., 2008). We hypothesize the melanopsin-associated collaterals provide the synaptic pathway by which the intrinsic, irradiance coding signal reaches the dopaminergic circuit.