Kainic acid에 의해 유발된 망막신경세포 손상에 대한 Betaxolol의 신경방어 효과
Neuroprotective effect of betaxolol on neuronal cell damage induced by kainic acid in rat retinas
망막신경세포 신경방어 BETAXOLOL 흥분독성자극;
- 원문 URL
Glutamate is a major excitatory neurotransmitter in the retina, and excessive stimulation on its receptors leads to widespread neuronal stress and death. In this study, I have investigated the protective effects of the topical -adrenoceptor antagonist Betoptic (0.25% betaxolol) in rat retina following neuronal cell damage induced by excitotoxicity of kainic acid (KA) injection. Like other areas of the central nervous system, the retina is highly vulnerable to KA-induced injury. A single dose of 3ul of 2mM KA was injected into the vitreous of rat eyes. After KA-injection, the thickness of the retinal layers and the immunoreactivities of choline acetyltransferase (ChAT) and tyrosine hydroxylase (TH) were examined. The morphometric analysis of retinal damage in KA-injected eyes showed significant cell loss in the inner nuclear layer (INL) and thinning of the inner plexiform layer (IPL) of the retina, but not of other retinal layers (ONL). In addition, the ChAT and TH immunoreactivity had almost completely disappeared in the retinas 7 days after the KA injection. These results suggest that the inner retinal layers are more susceptible to KA-induced injury than the outer retinal layer. Histological examination demonstrated protective effects of betaxolol on KA-induced retinal damage, which was more substantial in the inner retina layer. When two drops of betaxolol, once before KA injection and twice daily for 7 days after KA injection, were continuously administered, the reductions in the retinal ChAT, TH immunoreactivities and the thickness of the retinal layers were significantly attenuated. The present study suggests that topically applied betaxolol is an efficient neuroprotective agent which prevents the retinal cell damage induced by KA injection in rats.