Srivastava Prerna, Sinha-Mahapatra Sumit K, Ghosh Abhinaba, Srivastava Ipsit, Dhingra Narender K
National Brain Research Centre, Manesar (Gurgaon) Haryana, India.
PLoS One. 2015 Apr 2;10(4):e0123896. doi: 10.1371/journal.pone.0123896. eCollection 2015.
Loss of photoreceptors leads to significant remodeling in inner retina of rd1 mouse, a widely used model of retinal degeneration. Several morphological and physiological alterations occur in the second- and third-order retinal neurons. Synaptic activity in the excitatory bipolar cells and the predominantly inhibitory amacrine cells is enhanced. Retinal ganglion cells (RGCs) exhibit hyperactivity and aberrant spiking pattern, which adversely affects the quality of signals they can carry to the brain. To further understand the pathophysiology of retinal degeneration, and how it may lead to aberrant spiking in RGCs, we asked how loss of photoreceptors affects some of the neurotransmitter receptors in rd1 mouse. Using Western blotting, we measured the levels of several neurotransmitter receptors in adult rd1 mouse retina. We found significantly higher levels of AMPA, glycine and GABAa receptors, but lower levels of GABAc receptors in rd1 mouse than in wild-type. Since GABAa receptor is expressed in several retinal layers, we employed quantitative immunohistochemistry to measure GABAa receptor levels in specific retinal layers. We found that the levels of GABAa receptors in inner plexiform layer of wild-type and rd1 mice were similar, whereas those in outer plexiform layer and inner nuclear layer combined were higher in rd1 mouse. Specifically, we found that the number of GABAa-immunoreactive somas in the inner nuclear layer of rd1 mouse retina was significantly higher than in wild-type. These findings provide further insights into neurochemical remodeling in the inner retina of rd1 mouse, and how it might lead to oscillatory activity in RGCs.
光感受器的丧失会导致rd1小鼠(一种广泛使用的视网膜变性模型)的视网膜内层发生显著重塑。视网膜第二级和第三级神经元会出现几种形态和生理变化。兴奋性双极细胞和主要为抑制性的无长突细胞的突触活动增强。视网膜神经节细胞(RGCs)表现出活动亢进和异常的放电模式,这会对它们向大脑传递信号的质量产生不利影响。为了进一步了解视网膜变性的病理生理学,以及它如何导致RGCs异常放电,我们研究了光感受器的丧失如何影响rd1小鼠中的一些神经递质受体。我们使用蛋白质免疫印迹法测量了成年rd1小鼠视网膜中几种神经递质受体的水平。我们发现,与野生型相比,rd1小鼠中AMPA、甘氨酸和GABAa受体的水平显著更高,但GABAc受体的水平更低。由于GABAa受体在视网膜的多个层中表达,我们采用定量免疫组织化学方法测量特定视网膜层中GABAa受体的水平。我们发现,野生型和rd1小鼠内网状层中GABAa受体的水平相似,而在rd1小鼠中,外网状层和内核层中的GABAa受体水平更高。具体而言,我们发现rd1小鼠视网膜内核层中GABAa免疫反应性胞体的数量显著高于野生型。这些发现为rd1小鼠视网膜内层的神经化学重塑以及它如何导致RGCs的振荡活动提供了进一步的见解。