Endogenous neuroprotection in the retina

Abstract

Ischemic preconditioning (IPC) protects the rat retina against the injury that ordinarily follows severe ischemia. The retina is protected against the damage following severe ischemia for up to 72h after the application of IPC. However, there is no early preconditioning, i.e. protective effects starting within hours of preconditioning. The IPC stimulus consists of a brief, non-damaging period of ischemia. It results in complete preservation of retinal structure and function following ischemia, and is thus the most robust neuroprotection demonstrated in the retina to date. Release of adenosine, de novo protein synthesis, and mediators such as protein kinase C and K(+) ATP channels are required for IPC protection. Both the adenosine A1 and A2a receptors are involved. However, the molecular mechanisms for neuroprotection have not been completely described. It appears that both increased expression of protective proteins and decreased expression of pro-apoptotic proteins are involved. In addition, IPC prevents hypoperfusion following severe ischemia. Further study of the IPC phenomenon could lead to an enhanced understanding of the mechanisms of ischemic damage and its prevention in the retina.