德国和奥地利一个联合研究小组发现，在甲状腺激素的调控下，成年老鼠的视网膜锥细胞中能产生不同的视觉色素。他们认为，这一机制可能存在于人类等所有哺乳动物中，因此成人甲状腺激素缺乏也会影响他们的色彩识别能力。
视网膜锥体细胞荧光显微照片
成年健康大鼠(顶部)和甲状腺激素不足的大鼠(底部)
在视网膜中，视锥细胞负责识别颜色。大部分哺乳动物有两种光谱的视锥细胞类型，都包含了两种视觉色素（视蛋白），一种对短波光（紫外/蓝视蛋白）敏感，另一种对中长波光（绿视蛋白）敏感。视锥细胞会表达一种甲状腺激素受体，通过激素来抑制紫外/蓝视蛋白的合成，而激活绿视蛋白的合成。此前的研究认为，甲状腺激素控制视蛋白合成只是发育中的自然现象，随着机体发育，成熟视锥细胞中会建立起一套确定的“视蛋白程序”，不需要进一步调控。
但最近，德国马普研究院法兰克福脑研究所与法兰克福大学以及奥地利维也纳的几家大学联合，研究了在小鼠出生后早期发育期间甲状腺激素水平对视锥细胞的影响。结果发现，激素的影响会持续很长时间，在小鼠出生几周以后，激素影响仍然存在。
据研究小组分析，成熟小鼠甲状腺功能衰退几周后，它的视锥细胞就会受到影响，所有视锥细胞转化为合成紫外/蓝视蛋白，绿视蛋白合成减少。经治疗激素水平恢复正常以后，视锥细胞也会还原成以前的样子，继续按“规定”工作：一种合成绿视蛋白，另一种合成紫外/蓝视蛋白。两种视锥细胞在整个生命期间都受甲状腺激素的调控并且过程可逆。
马普研究院研究所的马丁·格鲁斯曼说，如果该机制在人类视锥细胞中也如此，新发现在临床上具有重要意义。由饮食或甲状腺切除造成的成人甲状腺激素缺乏，将会影响他们的视蛋白合成与色彩识别能力。（生物谷Bioon.com）
生物谷推荐英文摘要：
Journal of Neuroscience, 31(13): 4844-4851 (March 30, 2011) DOI: 10.1523/JNEUROSCI.6181-10.2011
Thyroid hormone controls cone opsin expression in the retina of adult rodents
Anika Glaschke, Jessica Weiland, Domenico Del Turco, Marianne Steiner, Leo Peichl, Martin Glösmann
Mammalian retinas display an astonishing diversity in the spatial arrangement of their spectral cone photoreceptors, probably in adaptation to different visual environments. Opsin expression patterns like the dorsoventral gradients of short-wave-sensitive (S) and middle- to long-wave-sensitive (M) cone opsin found in many species are established early in development and thought to be stable thereafter throughout life. In mouse early development, thyroid hormone (TH), through its receptor TRβ2, is an important regulator of cone spectral identity. However, the role of TH in the maintenance of the mature cone photoreceptor pattern is unclear. We here show that TH also controls adult cone opsin expression. Methimazole-induced suppression of serum TH in adult mice and rats yielded no changes in cone numbers but reversibly altered cone patterns by activating the expression of S-cone opsin and repressing the expression of M-cone opsin. Furthermore, treatment of athyroid Pax8?/? mice with TH restored a wild-type pattern of cone opsin expression that reverted back to the mutant S-opsin-dominated pattern after termination of treatment. No evidence for cone death or the generation of new cones from retinal progenitors was found in retinas that shifted opsin expression patterns. Together, this suggests that opsin expression in terminally differentiated mammalian cones remains subject to control by TH, a finding that is in contradiction to previous work and challenges the current view that opsin identity in mature mammalian cones is fixed by permanent gene silencing
