Article ID Journal Published Year Pages File Type
4348461 Neuroscience Letters 2008 5 Pages PDF
Abstract

In response to mild ischemic stress, the brain elicits endogenous survival mechanisms to protect cells against a subsequent lethal ischemic stress, referred to as ischemic tolerance. The molecular signals that mediate this protection are thought to involve the expression and activation of multiple kinases, including protein kinase C (PKC). Here we demonstrate that ɛPKC mediates cerebral ischemic tolerance in vivo. Systemic delivery of ψɛRACK, an ɛPKC-selective peptide activator, confers neuroprotection against a subsequent cerebral ischemic event when delivered immediately prior to stroke. In addition, activation of ɛPKC by ψɛRACK treatment decreases vascular tone in vivo, as demonstrated by a reduction in microvascular cerebral blood flow. Here we demonstrate the role of acute and transient ɛPKC in early cerebral tolerance in vivo and suggest that extra-parenchymal mechanisms, such as vasoconstriction, may contribute to the conferred protection.

Related Topics
Life Sciences Neuroscience Neuroscience (General)
Authors
, , , , ,