Investigative ophthalmology & visual science · 2007
Neuroprotective effect of transcorneal electrical stimulation on the acute phase of optic nerve injury.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Miyake Ken-ichiro, Yoshida Miho, Inoue Yoshitsugu, Hata Yoshio
Аннотация
PURPOSE: Traumatic optic neuropathy often induces a loss of vision that proceeds rapidly within several hours, together with retinal ganglion cell death, in a much slower time course. Electrical stimulation has previously been shown to rescue injured retinal ganglion cells from cell death. The present study tests whether transcorneal electrical stimulation could preserve visual function after an optic nerve crush.
METHODS: Transcorneal electrical stimulation was given immediately after a calibrated optic nerve crush. We measured visually evoked potentials (VEPs) in the visual cortex of rats before and immediately after the optic nerve crush and after the transcorneal stimulation to estimate an extent of damage and effects of stimulation in individual animals. In addition, the retinal axons were labeled with a fluorescent anterograde tracer to determine whether the transcorneal electrical stimulation can protect the retinal axons from degeneration.
RESULTS: The optic nerve crush was made at an intensity that does not allow a spontaneous recovery of VEP for 1 week. The transcorneal stimulation immediately increased VEP amplitude impaired by the optic nerve crush, and this augmentation was often preserved after 1 week. In the stimulated animals, a larger amount of retinal axons projected centrally beyond the crushed region in comparison to the unstimulated animals.
CONCLUSIONS: Transcorneal electrical stimulation would restore the functional impairment of optic nerve by traumatic injury at a very early stage and protect retinal axons from the ensuing degeneration.
METHODS: Transcorneal electrical stimulation was given immediately after a calibrated optic nerve crush. We measured visually evoked potentials (VEPs) in the visual cortex of rats before and immediately after the optic nerve crush and after the transcorneal stimulation to estimate an extent of damage and effects of stimulation in individual animals. In addition, the retinal axons were labeled with a fluorescent anterograde tracer to determine whether the transcorneal electrical stimulation can protect the retinal axons from degeneration.
RESULTS: The optic nerve crush was made at an intensity that does not allow a spontaneous recovery of VEP for 1 week. The transcorneal stimulation immediately increased VEP amplitude impaired by the optic nerve crush, and this augmentation was often preserved after 1 week. In the stimulated animals, a larger amount of retinal axons projected centrally beyond the crushed region in comparison to the unstimulated animals.
CONCLUSIONS: Transcorneal electrical stimulation would restore the functional impairment of optic nerve by traumatic injury at a very early stage and protect retinal axons from the ensuing degeneration.