Abstract
Purpose :
The retina is known as a highly metabolic tissue. Using light-induced retinal degeneration model mice, we evaluated the neuroprotective effect of activated AMP-activated protein kinase (AMPK) which plays a crucial role in metabolism.
Methods :
Seven- to 8-week-old BALB/c mice were divided into 4 groups and treated either with control vehicle or an AMPK activator, 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) at 125 or 250 or 500 mg/kg body weight, twice, before and after 12 hours of dark adaptation. The mice were then, exposed to a white fluorescent lamp for 1 hour at 3000 lux. The TUNEL positive and apoptotic cells were counted in the retina 2 days after light exposure. Full-field scotopic electroretinogram was recorded in response to the flash light stimuli at intensities ranging from −2.12 to 2.89 log cds/m2, 4 days after the exposure.
Results :
The TUNEL positive and apoptotic cells were only found in the photoreceptor layer. The increase in the number of apoptotic cells in the light exposed retina was suppressed by AICAR. The decrease in the amplitudes of a-waves 4 days after light exposure was attenuated by in the AICAR treated group in a dose dependent manner. Along with this, decreased in b-wave amplitudes were also attenuated in the AICAR treated group under some of the stimulus condition. There were no changes in the implicit times of a-wave and b-wave.
Conclusions :
Both histological and functional analyses showed suppression of photoreceptor degeneration induced by light exposure in the AICAR treated group. Although further studies are required, AMPK activation may have a neuroprotective effect against light-induced photoreceptor degeneration.
This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.