Transient focal
ischemia induced in rat brain by occlusion of the middle cerebral artery (MCAo) elicits a generalized induction of the 72 kDa
heat-shock protein (hsp72) heralding functional recovery. As this effect implies activation of
protein synthesis, and local systems of
protein synthesis are present in brain synapses, and may be analyzed in preparations of brain synaptosomes, we evaluated hsp72 expression and
protein synthesis in synaptosomal fractions of spontaneously hypertensive rats (SHRs) subjected to permanent MCAo. SHRs were randomly divided in ischemics and
sham controls, anaesthesia controls and passive controls. Focal
ischemia was induced under
chloral hydrate anaesthesia by unilateral permanent MCAo.
Protein synthesis was determined by [35S]
methionine incorporation into synaptosomal
proteins from ischemic and contralateral cortex/striatum, and from cerebellum. Hsp72 expression was measured in the same fractions by immunoblotting. Our data demonstrate that under these conditions synaptic hsp72 markedly increases in the ischemic hemisphere 1 and 2 days after MCAo, progressively declining in the following 2 days, while no significant change occurs in control rats. In addition, in the ischemic hemisphere the rate of synaptic
protein synthesis increases more than two-fold between 1 and 4 days after MCAo, without showing signs of an impending decline. The present data provide the first demonstration that synaptic
protein synthesis is massively involved in brain
plastic events elicited by permanent focal
ischemia.