Neurotoxic and cytoprotective mechanisms in the ischemic neocortex.

Neuronal damage in ischemic stroke occurs due to permanent imbalance between the metabolic needs of the brain and the ability of the blood-vascular system to maintain glucose delivery and adequate gas exchange. Oxidative stress and excitotoxicity trigger complex processes of neuroinflammation, necrosis, and apoptosis of both neurons and glial cells. This review summarizes data on the structural and chemical changes in the neocortex and main cytoprotective effects induced by focal ischemic stroke.

Topography of neurotrophins in the rat neocortex and their role in neuron apoptosis after experimental ischemic stroke.

Neuronal loss due to apoptosis after ischemic injury depends on the trophic support of neurons and cytoprotective effects of neurotrophins (NTs). Different NTs may activate both pro- and antiapoptotic factors. Their distribution in the ischemic core (IC) and penumbra (IP) has been poorly studied.