Abstract

Anterior ischemic optic neuropathy (AION) is an important cause of acute vision loss in adults, and there is no effective treatment. We studied early changes following experimental AION and tested the benefit of a potential treatment.Materials andWe induced experimental AION in adult mice and tested the effects of short-term (daily for 3 days) and long-term (every other day for 3 weeks) aB-crystallin (aBC) treatment using histological and serial intracranial flash visual evoked potential recordings.One day after experimental AION, there was swelling at the optic nerve (ON) head and increased expression of aBC, a small heat shock protein important in ischemia and inflammation. This upregulation coincided with microglial and astrocytic activation. Our hypothesis was that aBC may be part of the endogenous protective mechanism against injury, thus we tested the effects of aBC on experimental AION. Daily intraveneous or intravitreal aBC injections did not improve visual evoked potential amplitude or latency at days 1-2. However, aBC treatment decreased swelling and dampened the microglial and astrocytic activation on day 3. Longer treatment with intravenous aBC led to acceleration of visual evoked potential latency over 3 weeks, without improving amplitude. This latency acceleration did not correlate with increased retinal ganglion cell survival but did correlate with complete rescue of the ON oligodendrocytes, which are important for myelination.We identified aBC as an early marker following experimental AION. Treatment with aBC enhanced this endogenous, post-ischemic response by decreasing microglial activation and promoting ON oligodendrocyte survival.

View details for DOI 10.1038/eye.2011.42

View details for Web of Science ID 000291430100020

View details for PubMedID 21475310

View details for PubMedCentralID PMC3178147