表現視黑質之視神經細胞藉視網膜內之軸突分支接觸無軸突細胞

Abstract

視網膜的結構與神經迴路已經被研究了一百多年。傳統認知中訊號如此傳遞：視桿細胞與視椎細胞接收光訊號並且轉換為神經衝動，將訊號傳遞至水平細胞、無軸突細胞與雙極細胞，並且藉由視神經細胞傳遞到腦。近期研究指出除了上述的路徑之外，一類視神經細胞，即自主感光視神經細胞，能夠藉由未知的方式傳遞回饋訊號至上游部分種類的無軸突細胞。其他研究也指出自主感光視神經細胞具有視網膜內的軸突分支，深入是網膜中的內網狀層，然而這些軸突分支的型態與功能等都尚未被發掘。藉由基因轉殖與隨機標定小鼠視網膜上的自主感光視神經細胞，我們發現兩組型態各異的軸突分枝；此外我們也發現這些軸突分枝會與多巴胺無軸突細胞產生神經連結。我們的實驗結果支持自主感光神經細胞能夠藉由軸突分枝將訊號傳給無軸突細胞，並且可能藉此進一步影響視網膜的功能。

Retinal structure and functional circuits have been studied for more than a century. It is well known that the information flow of retinal circuit starts form light reception by rods and cones, to horizontal cells, amacrine cells and bipolar cells, and transduces to brain by retinal ganglion cells. However, recent studies indicated that a group of melanopsin containing retinal ganglion cells, named intrinsically photosensitive retinal ganglion cells (ipRGCs), send feedback signal to specific sub-population of amacrine cells by an unknown mechanism. Recent studies showed that ipRGC contain intra-retinal axon collaterals that stratified in the inner plexiform layer, yet the morphology and functions of these collaterals remain unclear. By randomly genetic labeling of ipRGCs in mice, our study shows two morphologically distinct types of ipRGC intra-retinal axon collaterals. We also found those collaterals connect to dopaminergic amacrine cells. Our finding suggests that ipRGCs send feedback signal to amacrine cells via intra-retinal collaterals, which may modulate retinal functions.