Constitutive nitric oxide synthase activity is required to trigger ischemic tolerance in mouse retina.

Profound morphologic and functional protection against retinal ischemic injury can be achieved if the tissue is 'preconditioned' one day earlier with a brief, noninjurious ischemic challenge. To begin to address the mechanistic basis of this 'ischemic tolerance', we used genetic and pharmacologic approaches to test the hypothesis that nitric oxide (NO) derived from one of the three NO synthase (NOS) isoforms was responsible for triggering the adaptive response to brief preconditioning ischemia. Retinae of adult mice were preconditioned with 5-min preconditioning ischemia and subjected to 45-min injurious ischemia 24 hr later.

Mouse models of retinal ischemic tolerance.

Purpose: A brief period of noninjurious retinal ischemia, termed preconditioning, has been documented in rats to afford transient protection from retinal ischemic injury, a phenomenon known as ischemic tolerance. The present study was undertaken to develop and systematically characterize mouse models of ischemic tolerance.

Methods: Retinal ischemic injury was caused by elevating intraocular pressure for 30, 45, or 60 minutes in chloral hydrate-anesthetized ND4 Swiss-Webster mice.

Synucleins in glaucoma: implication of gamma-synuclein in glaucomatous alterations in the optic nerve.

Synucleins are small proteins associated with neurodegenerative diseases and some forms of cancer. They are studied predominantly in the brain; information about their presence and functions in ocular tissues is scarce. Here we describe the localization of three members of the synuclein family in the optic nerve of donors with different types of glaucoma compared with control samples from donors without ocular diseases.