Fischer A J, McGuire J J, Schaeffel F, Stell W K
Department of Anatomy, Neuroscience Research Group, University of Calgary Faculty of Medicine, 3330 Hospital Drive N.W., Calgary, Alberta T2N 4N1, Canada.
Nat Neurosci. 1999 Aug;2(8):706-12. doi: 10.1038/11167.
Ocular growth and refraction are regulated by visual processing in the retina. We identified candidate regulatory neurons by immunocytochemistry for immediate-early gene products, ZENK (zif268, Egr-1) and Fos, after appropriate visual stimulation. ZENK synthesis was enhanced by conditions that suppress ocular elongation (plus defocus, termination of form deprivation) and suppressed by conditions that enhance ocular elongation (minus defocus, form deprivation), particularly in glucagon-containing amacrine cells. Fos synthesis was enhanced by termination of visual deprivation, but not by defocus and not in glucagon-containing amacrine cells. We conclude that glucagon-containing amacrine cells respond differentially to the sign of defocus and may mediate lens-induced changes in ocular growth and refraction.
眼球的生长和屈光受视网膜视觉处理的调节。我们通过免疫细胞化学方法,针对早期即刻基因产物ZENK(zif268,Egr-1)和Fos,在适当的视觉刺激后鉴定出候选调节神经元。抑制眼球伸长的条件(加散焦、剥夺形觉终止)可增强ZENK的合成,而增强眼球伸长的条件(减散焦、形觉剥夺)则抑制ZENK的合成,尤其是在含胰高血糖素的无长突细胞中。视觉剥夺终止可增强Fos的合成,但散焦不会增强,且在含胰高血糖素的无长突细胞中也不会增强。我们得出结论,含胰高血糖素的无长突细胞对散焦的正负反应不同,可能介导晶状体诱导的眼球生长和屈光变化。