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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.

It has been shown that a three-week feeding of rats with oil derived from seeds of amaranth (Amaranthus cruentus L.) leads to a moderate activation of respiration of coupled and uncoupled rat liver mitochondria (MCh) that oxidize succinate and succinate + glutamate, as well as alpha-ketoglutarate and alpha-ketoglutarate + malonate. In animals receiving the amaranth oil, the injection of adrenaline did not affect the oil-activated respiration of MCh during succinate oxidation; i. e., animals prepared by an oil-enriched diet were resistant to the action of adrenaline, which prevented from possible hyperactivation of mitochondrial functions. In the group of control animals, which received no oil, the injection of adrenaline activated the rate of phosphorylating respiration of MCh during oxidation of succinate or succinate + glutamate: the rate of oxygen uptake in state 3 respiration (by Chance) increased, and the phosphorylation time decreased. The injection of adrenaline did not affect the parameters of respiration of MCh that oxidize a-ketoglutarate; however, in the presence of malonate, the oxidation of alpha-ketoglutarate in state 3 and uncoupled respiration have shown mild but significant increase in response to adrenaline. In animals receiving the amaranth oil, the oil-induced activation of respiration of MCh in response to adrenaline retained but did not increase; however, the phosphorylation time significantly decreased. Thus, concentrated oil of seeds activates the respiration of MCh. In addition, it enhances an energetic function of MCh, which prevents from the hyper-activation of mitochondrial respiration by adrenaline. Therefore an activation of energetic function of MCh by amaranth oil could explain its adaptogenic effect on rats.