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Experiments on the model of bilateral photothrombosis in the prefrontal cortex showed that antibodies to glutamate administered intranasally 1 h after ischemic damage to the brain cortex led to a decrease in glutamate content in the hippocampus and prefrontal cortex and had no effect on aspartate concentration in these structures of the brain.

Experiments were performed on rats with bilateral photothrombosis of vessels in the prefrontal cortex. Intranasal administration of antibodies to glutamate (1 h after ischemia of the brain cortex) improved retention of conditioned passive avoidance response, which was elicited before ischemic damage. The content of antibodies to glutamate in the serum of rats increased significantly on day 8 after bilateral photochemical thrombosis of vessels in the prefrontal cortex compared to that in the control.

The prefrontal (cognitive) cerebral cortex of rats was studied by morphological and physiological methods 56 days after stroke induced by photothrombosis. The cognitive capacity impaired after the intervention was completely restored by this time. The count of fused cells (dikaryons) increased significantly in experimental and sham-operated (control) animals in comparison with the early period (7 days) after surgery. Normalization of the dikaryon and mononuclear cell structure was observed after 56 days. Presumably, cell fusion promotes their morphological restoration and regeneration of the lost functional capacity. Fusion is regarded as a manifestation of physiological and reparative regeneration of the cortex.

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.