Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8791905 | Experimental Eye Research | 2018 | 44 Pages |
Abstract
Neuromyelitis optica spectrum disorders (NMOSD) are a group of autoimmune astrocytopathies in the central nervous system, which are mainly caused by immunoglobulin G (IgG) against astrocyte water channel aquaporin-4 (AQP4). In this study, we aimed to establish a model of NMOSD-related optic neuritis (NMOSD-ON) and to evaluate the progressive changes of the optic nerve and visual function. AQP4 IgG-positive serum from NMOSD patients was injected into the subarachnoid space of the rat optic nerve to induce the NMOSD-ON model (AQP4Â +Â group), and healthy serum was injected as the control. The visual evoked potential, pupillary light reflex and optical coherence tomography were monitored every week for 3 weeks after induction. Compared with the control group, the amplitude of the N1-P1 peak and pupillary light reflex in the AQP4+ group were reduced within the first week and then remained low thereafter. Consistent with the functional deficits, the thickness of the peripapillary retinal nerve fiber layer in the AQP4Â +Â group was also greatly reduced. At the end of 3 weeks, there was a loss of retinal ganglion cells and the optic nerves showed characteristic NMOSD-like pathologic changes, including deposition of AQP4 IgG, local astrocyte damage, demyelination, microglia activation, macrophage infiltration and axonal injury. Thus, we have established an NMOSD-ON rat model with deficits in the optic nerve and visual function that may be a valuable tool for exploring the mechanism of NMOSD-ON and evaluating its potential therapeutic treatment.
Keywords
Related Topics
Life Sciences
Immunology and Microbiology
Immunology and Microbiology (General)
Authors
Yuxin Zhang, Yiqin Bao, Wei Qiu, Lisheng Peng, Ling Fang, Ying Xu, Hui Yang,