Hou Baoke, Fu Yan, Weng Chuanhuang, Liu Weiping, Zhao Congjian, Yin Zheng Qin
Southwest Hospital/Southwest Eye Hospital, Third Military Medical UniversityChongqing, China.
Department of Ophthalmology, Chinese PLA General HospitalBeijing, China.
Front Cell Neurosci. 2017 Apr 20;11:98. doi: 10.3389/fncel.2017.00098. eCollection 2017.
Rod-cone gap junctions open at night to allow rod signals to pass to cones and activate the cone-bipolar pathway. This enhances the ability to detect large, dim objects at night. This electrical synaptic switch is governed by the circadian clock and represents a novel form of homeostatic plasticity that regulates retinal excitability according to network activity. We used tracer labeling and ERG recording in the retinae of control and retinal degenerative dystrophic RCS rats. We found that in the control animals, rod-cone gap junction coupling was regulated by the circadian clock via the modulation of the phosphorylation of the melatonin synthetic enzyme arylalkylamine N-acetyltransferase (AANAT). However, in dystrophic RCS rats, AANAT was constitutively phosphorylated, causing rod-cone gap junctions to remain open. A further b/a-wave ratio analysis revealed that dystrophic RCS rats had stronger synaptic strength between photoreceptors and bipolar cells, possibly because rod-cone gap junctions remained open. This was despite the fact that a decrease was observed in the amplitude of both a- and b-waves as a result of the progressive loss of rods during early degenerative stages. These results suggest that electric synaptic strength is increased during the day to allow cone signals to pass to the remaining rods and to be propagated to rod bipolar cells, thereby partially compensating for the weak visual input caused by the loss of rods.
视杆 - 视锥细胞间隙连接在夜间开放，使视杆细胞的信号传递给视锥细胞并激活视锥 - 双极细胞通路。这增强了在夜间检测大的暗物体的能力。这种电突触开关受生物钟控制，代表了一种新型的稳态可塑性形式，可根据网络活动调节视网膜兴奋性。我们在对照和视网膜退行性营养不良的RCS大鼠的视网膜中使用了示踪剂标记和视网膜电图记录。我们发现，在对照动物中，视杆 - 视锥细胞间隙连接耦合受生物钟通过调节褪黑素合成酶芳基烷基胺N - 乙酰基转移酶（AANAT）的磷酸化来调控。然而，在营养不良的RCS大鼠中，AANAT持续磷酸化，导致视杆 - 视锥细胞间隙连接保持开放。进一步的b/a波比率分析显示，营养不良的RCS大鼠在光感受器和双极细胞之间具有更强的突触强度，这可能是因为视杆 - 视锥细胞间隙连接保持开放。尽管在早期退化阶段由于视杆细胞的逐渐丧失，a波和b波的振幅均有所下降，但情况依然如此。这些结果表明，白天电突触强度增加，以使视锥细胞信号传递给剩余的视杆细胞并传播到视杆双极细胞，从而部分补偿因视杆细胞丧失而导致的微弱视觉输入。
