No abstract

The expression of mitochondrial protein UCP2 and cytochrome C-oxidase subunit III genes in the hippocampus and prefrontal cortex was evaluated by real-time PCR 3 and 7 days after microinjection of kainic acid into the dorsal hippocampus. In contrast to cytochrome C-oxidase subunit III mRNA, the level of UCP2 mRNA in the hippocampus increased 1 week after microinjection of kainic acid. The expression of both genes in the prefrontal cortex did not differ from the control. Presumably, activation of UCP2 synthesis in hippocampal injury indicates the neuroprotective effects of this protein.

The expression of synaptophysin (vesicular protein) and mGluR5 (metabotropic glutamate receptor) genes was studied 3, 7, and 20 days after cainic acid injury of the dorsal hippocampal area in Wistar rats. The expression of both genes was characteristically reduced in the hippocampus. Twenty days after the exposure the expression of mGluR5 in this brain area reached the control level, while synaptophysin expression remained low. An opposite trend was observed in the frontal cortex: synaptophysin expression 20 days after exposure did not differ from the control, while mGluR5 expression was reduced. The peculiar time course of both genes' expression in the hippocampus and frontal cortex indicates the involvement of the frontal cortex in mechanisms of functional recovery after hippocampal injuries.

No abstract

We studied behavioral reactions of rats after injection of subconvulsive dose of kainic acid into the frontal cortex and mitochondrial respiration in the hippocampus and frontal and temporal cortex 17-20 days after administration of kainic acid. Retention of acquired habit and the dynamics of its extinction in experimental rats were close to those in the control group. Changes in mitochondrial function were observed only in the region of kainic acid injection: activation of phosphorylating respiration during oxidation of succinate. Presumably, the detected activation of energy metabolism in the frontal cortex indicates functional restructuring in mitochondria, aimed at compensation of disorders caused by the neurotoxin.