Our goal was to investigate the neuroprotective effects of galantamine in a mouse model of blast-induced indirect traumatic optic neuropathy (bITON). Galantamine is an FDA-approved acetylcholinesterase inhibitor used to treat mild-moderate Alzheimer's disease. We exposed one eye of an anesthetized mouse to repeat bursts of over-pressurized air to induce traumatic optic neuropathy. Mice were given regular or galantamine-containing water (120 mg/L) ad libitum, beginning immediately after blast and continuing for one month. Electroretinograms and visual evoked potentials were performed just prior to endpoint collection. Histological and biochemical assessments were performed to assess activation of sterile inflammation, axon degeneration, and synaptic changes. Galantamine treatment mitigated visual function deficits induced by our bITON model via preservation of the b-wave of the electroretinogram and the N1 of the visual evoked potential. We also observed a reduction in axon degeneration in the optic nerve as well as decreased rod bipolar cell dendritic retraction. Galantamine also showed anti-inflammatory and antioxidant effects. Galantamine may be a promising treatment for blast-induced indirect traumatic optic neuropathy as well as other optic neuropathies.

中文翻译：

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加兰他敏可防止实验性神经创伤中的突触、轴突和视力缺陷。

我们的目标是研究加兰他敏对爆炸引起的间接创伤性视神经病变 (bITON) 小鼠模型的神经保护作用。加兰他敏是 FDA 批准的一种乙酰胆碱酯酶抑制剂，用于治疗轻中度阿尔茨海默病。我们将麻醉小鼠的一只眼睛暴露于重复的高压空气中，以诱发创伤性视神经病变。小鼠在爆炸后立即开始随意饮用普通水或含加兰他敏的水（120 mg/L），持续一个月。在终点收集之前进行视网膜电图和视觉诱发电位。进行组织学和生化评估以评估无菌炎症的激活、轴突变性和突触变化。加兰他敏治疗通过保留视网膜电图的 b 波和视觉诱发电位的 N1 来减轻由我们的 bITON 模型引起的视功能缺陷。我们还观察到视神经轴突变性的减少以及杆双极细胞树突回缩的减少。加兰他敏还表现出抗炎和抗氧化作用。加兰他敏可能是治疗爆炸引起的间接创伤性视神经病变以及其他视神经病变的有希望的治疗方法。