Departamento de Oftalmología, Facultad de Medicina, Campus Universitario de Espinardo, Universidad de Murcia, 30100 Espinardo, Murcia, Spain.
Prog Retin Eye Res. 2012 Jan;31(1):1-27. doi: 10.1016/j.preteyeres.2011.08.001. Epub 2011 Sep 21.
Glaucoma, the second most common cause of blindness, is characterized by a progressive loss of retinal ganglion cells and their axons, with a concomitant loss of the visual field. Although the exact pathogenesis of glaucoma is not completely understood, a critical risk factor is the elevation, above normal values, of the intraocular pressure. Consequently, deciphering the anatomical and functional changes occurring in the rodent retina as a result of ocular hypertension has potential value, as it may help elucidate the pathology of retinal ganglion cell degeneration induced by glaucoma in humans. This paper predominantly reviews the cumulative information from our laboratory's previous, recent and ongoing studies, and discusses the deleterious anatomical and functional effects of ocular hypertension on retinal ganglion cells (RGCs) in adult rodents. In adult rats and mice, perilimbar and episcleral vein photocauterization induces ocular hypertension, which in turn results in devastating damage of the RGC population. In wide triangular sectors, preferentially located in the dorsal retina, RGCs lose their retrograde axonal transport, first by a functional impairment and after by mechanical causes. This axonal damage affects up to 80% of the RGC population, and eventually causes their death, with somal and intra-retinal axonal degeneration that resembles that observed after optic nerve crush. Importantly, while ocular hypertension affects the RGC population, it spares non-RGC neurons located in the ganglion cell layer of the retina. In addition, functional and morphological studies show permanent alterations of the inner and outer retinal layers, indicating that further to a crush-like injury of axon bundles in the optic nerve head there may by additional insults to the retina, perhaps of ischemic nature.
青光眼是第二大致盲原因，其特征是视网膜神经节细胞及其轴突进行性丧失，同时视野丧失。虽然青光眼的确切发病机制尚未完全了解，但一个关键的危险因素是眼内压升高到正常以上。因此，阐明由于眼高压而在啮齿动物视网膜中发生的解剖和功能变化具有潜在价值，因为它可能有助于阐明人类青光眼引起的视网膜神经节细胞变性的病理学。本文主要综述了我们实验室以前、最近和正在进行的研究的累积信息，并讨论了眼高压对成年啮齿动物视网膜神经节细胞（RGCs）的有害解剖和功能影响。在成年大鼠和小鼠中，眼周和巩膜静脉光凝术可引起眼高压，进而导致 RGC 群体毁灭性损伤。在宽三角形区域中，优先位于视网膜背部，RGC 失去逆行轴突运输，首先是功能障碍，然后是机械原因。这种轴突损伤影响高达 80%的 RGC 群体，最终导致它们死亡，伴随胞体和视网膜内轴突变性，类似于视神经挤压后观察到的情况。重要的是，虽然眼高压会影响 RGC 群体，但它会使位于视网膜神经节细胞层中的非 RGC 神经元免受影响。此外，功能和形态学研究表明内、外视网膜层的永久性改变，表明除了视神经头轴突束的挤压样损伤外，视网膜可能还受到其他损伤，可能是缺血性的。
