Genetic Dissection of Rod and Cone Pathways in the Dark-Adapted Mouse Retina
Genetic Dissection of Rod and Cone Pathways in the Dark-Adapted Mouse Retina
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DOI：
10.1152/jn.00142.2009
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发表时间：
2009-09-01
影响因子：
2.5
通讯作者：
Wu, Samuel M.
中科院分区：
文献类型：
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作者：
Abd-El-Barr, Muhammad M.;Pennesi, Mark E.;Wu, Samuel M.
Abd-El-Barr MM，Pennesi ME，Saszik SM，Barrow AJ，Lem J，Bramblett DE，Paul DL，Frishman LJ，Wu SM。暗适应小鼠视网膜视杆细胞和视锥细胞通路的遗传解剖。神经生理学杂志102：1945-1955,2009。2009年7月8日首次出版；DOI：10.1152/jn.00142.2009。哺乳动物视网膜的一项艰巨任务是编码动物在自然环境中经历的巨大范围(>；10(9)倍)的光强度。视网膜神经元通过将劳动划分为许多平行的视杆和视锥突触路径来执行这一任务。在这里，我们通过分析暗适应野生型、连接蛋白36基因敲除、去极化视杆双极细胞(DBCR)基因敲除和视杆转导α亚单位基因敲除小鼠的视网膜电信号(ERG)，主要是b波反应，研究了各种视杆和视锥细胞介导的通路的操作方案[WT，Cx36(-/-)，Bhlhb4(-/-)和Tr-α(-/-)]。为了进一步了解ERG不同成分的细胞起源，我们将暗适应ERG的反应与其他研究发表的暗适应小鼠视网膜的贴片电极记录的单个视网膜细胞的反应动态范围进行了比较。我们的结果提示，当光刺激较弱时，连接蛋白36介导的视杆细胞锥体偶联作用较弱，随着光刺激强度的增强而增强，视杆细胞信号可能通过直接的化学突触传递给DBC(C)S。此外，我们的分析表明，当刺激强到足以饱和杆状双极细胞的反应时，DBCR响应贡献了整个DBC响应的大约80%，而杆和锥体信号对整个DBC响应的贡献几乎相等。此外，我们的研究表明，暗适应、通路特异性突变体的ERGb波分析可以作为体内解剖视杆细胞和视锥突触通路的工具，并可用于研究视网膜通路特异性基因产物的功能。
Abd-El-Barr MM, Pennesi ME, Saszik SM, Barrow AJ, Lem J, Bramblett DE, Paul DL, Frishman LJ, Wu SM. Genetic dissection of rod and cone pathways in the dark-adapted mouse retina. J Neurophysiol 102: 1945-1955, 2009. First published July 8, 2009; doi:10.1152/jn.00142.2009. A monumental task of the mammalian retina is to encode an enormous range (> 10(9)-fold) of light intensities experienced by the animal in natural environments. Retinal neurons carry out this task by dividing labor into many parallel rod and cone synaptic pathways. Here we study the operational plan of various rod- and cone-mediated pathways by analyzing electroretinograms (ERGs), primarily b-wave responses, in dark-adapted wildtype, connexin36 knockout, depolarizing rod-bipolar cell (DBCR) knockout, and rod transducin alpha-subunit knockout mice [WT, Cx36(-/-), Bhlhb4(-/-),and Tr-alpha(-/-)]. To provide additional insight into the cellular origins of various components of the ERG, we compared dark-adapted ERG responses with response dynamic ranges of individual retinal cells recorded with patch electrodes from dark-adapted mouse retinas published from other studies. Our results suggest that the connexin36-mediated rod-cone coupling is weak when light stimulation is weak and becomes stronger as light stimulation increases in strength and that rod signals may be transmitted to some DBC(C)s via direct chemical synapses. Moreover, our analysis indicates that DBCR responses contribute about 80% of the overall DBC response to scotopic light and that rod and cone signals contribute almost equally to the overall DBC responses when stimuli are strong enough to saturate the rod bipolar cell response. Furthermore, our study demonstrates that analysis of ERG b-wave of dark-adapted, pathway-specific mutants can be used as an in vivo tool for dissecting rod and cone synaptic pathways and for studying the functions of pathway-specific gene products in the retina.