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PTEN expression regulates gap junction connectivity in the retina
Frontiers in Neuroanatomy ( IF 2.9 ) Pub Date : 2021-04-26 , DOI: 10.3389/fnana.2021.629244
Ashley M. Chen , Shaghauyegh S. Azar , Alexander Harris , Nicholas C. Brecha , Luis Pérez de Sevilla Müller

Manipulation of the phosphatase and tensin homolog (PTEN) pathway has been suggested as a therapeutic approach to treat or prevent vision loss due to retinal disease. In this study, we investigated the effects of deleting one copy of Pten in a well-characterized class of retinal ganglion cells called α-ganglion cells in the mouse retina. In Pten+/− retinas, α-ganglion cells did not exhibit major changes in their dendritic structure, although most cells developed a few, unusual loop-forming dendrites. By contrast, α-ganglion cells exhibited a significant decrease in heterologous and homologous gap junction mediated cell coupling with other retinal ganglion and amacrine cells. Additionally, the majority of OFF α-ganglion cells (12/18 cells) formed novel coupling to displaced amacrine cells. The number of connexin36 puncta, the predominant connexin that mediates gap junction communication at electrical synapses, was decreased by at least 50% on OFF α-ganglion cells. Reduced and incorrect gap junction connectivity of α-ganglion cells will affect their functional properties and alter visual image processing in the retina. The anomalous connectivity of retinal ganglion cells would potentially limit future therapeutic approaches involving manipulation of the Pten pathway for treating ganglion cell degeneration in diseases like glaucoma, traumatic brain injury, Parkinson’s and Alzheimer’s diseases.

中文翻译:

PTEN表达调节视网膜间隙连接的连通性

已经建议操纵磷酸酶和张力蛋白同源物(PTEN)途径作为治疗或预防由于视网膜疾病引起的视力丧失的治疗方法。在这项研究中,我们研究了在小鼠视网膜中,在特征明确的一类视网膜神经节细胞(称为α-神经节细胞)中删除一个拷贝的Pten的作用。在Pten +/-视网膜中,尽管大多数细胞会形成一些不寻常的环形成树突,但其神经节细胞的树突结构并未出现重大变化。相比之下,α-神经节细胞与其他视网膜神经节和无长突细胞的异源和同源间隙连接介导的细胞偶联显着降低。另外,大多数OFFα-神经节细胞(12/18细胞)与置换的无长突细胞形成新的偶联。连接蛋白36个点,介导电突触间隙连接通讯的主要连接蛋白在OFFα神经节细胞上降低了至少50%。α神经节细胞间隙连接的减少和不正确会影响它们的功能特性,并改变视网膜的视觉图像处理。视网膜神经节细胞的异常连通性可能会限制未来的治疗方法,包括操纵Pten途径治疗青光眼,脑外伤,帕金森氏症和阿尔茨海默氏病等神经节细胞变性。
更新日期:2021-04-27
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