德國和奧地利一個聯(lián)合研究小組發(fā)現(xiàn),，在甲狀腺激素的調(diào)控下，成年老鼠的視網(wǎng)膜錐細胞中能產(chǎn)生不同的視覺色素,。他們認為,，這一機制可能存在于人類等所有哺乳動物中,，因此成人甲狀腺激素缺乏也會影響他們的色彩識別能力。
視網(wǎng)膜錐體細胞熒光顯微照片
成年健康大鼠(頂部)和甲狀腺激素不足的大鼠(底部)
在視網(wǎng)膜中,，視錐細胞負責識別顏色,。大部分哺乳動物有兩種光譜的視錐細胞類型，都包含了兩種視覺色素（視蛋白）,，一種對短波光（紫外/藍視蛋白）敏感,，另一種對中長波光（綠視蛋白）敏感。視錐細胞會表達一種甲狀腺激素受體,，通過激素來抑制紫外/藍視蛋白的合成,，而激活綠視蛋白的合成。此前的研究認為,，甲狀腺激素控制視蛋白合成只是發(fā)育中的自然現(xiàn)象,，隨著機體發(fā)育，成熟視錐細胞中會建立起一套確定的“視蛋白程序”,，不需要進一步調(diào)控,。
但最近，德國馬普研究院法蘭克福腦研究所與法蘭克福大學以及奧地利維也納的幾家大學聯(lián)合,，研究了在小鼠出生后早期發(fā)育期間甲狀腺激素水平對視錐細胞的影響,。結(jié)果發(fā)現(xiàn)，激素的影響會持續(xù)很長時間,，在小鼠出生幾周以后,，激素影響仍然存在。
據(jù)研究小組分析,，成熟小鼠甲狀腺功能衰退幾周后,，它的視錐細胞就會受到影響，所有視錐細胞轉(zhuǎn)化為合成紫外/藍視蛋白,，綠視蛋白合成減少,。經(jīng)治療激素水平恢復正常以后，視錐細胞也會還原成以前的樣子,，繼續(xù)按“規(guī)定”工作：一種合成綠視蛋白,，另一種合成紫外/藍視蛋白。兩種視錐細胞在整個生命期間都受甲狀腺激素的調(diào)控并且過程可逆,。
馬普研究院研究所的馬丁·格魯斯曼說,，如果該機制在人類視錐細胞中也如此，新發(fā)現(xiàn)在臨床上具有重要意義,。由飲食或甲狀腺切除造成的成人甲狀腺激素缺乏,，將會影響他們的視蛋白合成與色彩識別能力。（生物谷Bioon.com）
生物谷推薦英文摘要：
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
