Photochemically induced thrombosis of blood vessels in the prefrontal cortex in rats was shown to lead to ischemic infarcts in the lesion zone. Bilateral ischemic lesioning of the prefrontal cortex degraded measures of spatial memory when animals were tested in a Morris water maze with an invisible platform 20-24 days after surgery. Chronic intranasal administration of the peptide Met-Glu-His-Phe-Pro-Gly-Pro (Semax), a synthetic analog of ACTH(4-7), at a dose of 250 microg/kg/day during the first six days after photothrombosis, led to recovery of the animals' learning ability. The long-term antiamnestic action of the peptide observed here may result from its neuroprotective activity and its ability to stimulate the synthesis of neurotrophic factors.
Semax had a pronounced neuroprotective and antiamnesic effect during focal photoinduced ischemia of the prefrontal cortex. Intranasal administration of Semax for 6 days decreased the volume of cortical infarction and improved retention and performance of conditioned passive avoidance response.
The neuroprotective and antiamnestic effects of GK-2 dipeptide (nerve growth factor mimetic) were studied on rats with photoinduced bilateral focal ischemia of the prefrontal cortex. Intraperitoneal injection of GK-2 in a dose of 1 mg/kg on days 1, 2, 4, and 6 postoperation led to a 62% reduction of cortical infarction volume on day 9 and completely preserved conditioned passive avoidance response trained before stroke.
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