Respiration and oxidative phosphorylation of the mitochondria of the brain of rats with various types of behavior

Livanova, L. M.; Sarkisova, K. Yu.; Luk’yanova, L. D.; Kolomeitseva, I. A.

doi:10.1007/bf01185442

Cited by 4 publications

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“…Moreover, during oxidation of the NAD-dependent substrates by the brain mitochondria of LR rats, the rate of electron transfer in the respiratory chain is the maximum and leads to exhaustion of the reserve potential of their respiratory activity, which is not observed in the brain of HR animals. The animals with different sensitivity to acute hypoxia under normoxic conditions and different organization of energy metabolism differ by the parameters of higher nervous activity [43].…”

Section: Time Course Of Respiratory Dysfunction In Hypoxiamentioning

confidence: 99%

Bioenergetic hypoxia: Definition, mechanisms, and methods of correction

Luk’yanova

1997

Bull Exp Biol Med

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Bioenergetic hypoxia is defined as a phasic process starting at the substrate site of the respiratory chain with injury to the mitochondrial enzymatic complex I and involving, as oxygen insufficiency progresses, the terminal cytochrome site of the respiratory chain. Different stages of the process, determined experimentally, are described from a bioenergetic viewpoint. The development of bioenergetic hypoxia in tissues of aninlals with different resistance to hypoxia is analyzed. Modern concepts of the trigger mechanisms of bioenergetic hypoxia and approaches to correcting the function of the energy system at different stages of hypoxia are discussed. Key Words: bioenergetic hypoxia; energy metabolism; respiratory enzymatic complexes; individual sensitivity to hypoxia; adaptation; antihypoxantsHypoxia is a highly prevalent phenomenon, which develops both under conditions of oxygen deficiency in the environment and as a result of a variety of diseases involving the respiratory and cardiovascular systems and impairing blood transporting function. All such disorders lead to a decrease in oxygen delivery to tissues to a level which is insufficient for maintaining function, metabolism, and structure of the cell. Thus, hypoxia is an important problem of practical and theoretical medicine.This problem has been researched for more than a hundred years. In Russia it attracted the attention of I. M. Sechenov, V. V. Pashutin, P. M. Al'bitskii, and E. A. Kartashevskii. Later it became the main object of research for N. N. Sirotinin, A. M. Charnyi, I. R. Petrov, Z. I. Barbashova, M. N. Gaevskaya, and lnany others. Due to these investigations, stndy of hypoxic states became an important branch of fundamental and applied medicine, which still remains a priority trend for the Russian science. At Department of Bioenergetics, Institute of Pharmacology, Russian Academy of Medical Sciences, Moscow present, a vast data bank on the mechanisms of hypoxia has been accumulated, permitting the creation of classifications of hypoxic states, development of prognostic criteria for assessing them, and analysis of the succession of disorders occurring under conditions Of oxygen deficiency.The intricate time course of this process and involvement of a wide spectrum of functional and metabolic systems regulating it at different levels of organization determine the multiplicity of the limiting sites and mechanisms underlying hypoxia. This l~act explains why, despite an almost lO0-year history of investigation, many pathogenetic aspects of hypoxia and many questions in antihypoxic defense are still not solved.The crucial factor leading to the development of h3rpoxic states is oxygen delivery from tile environment to the cell, where it participates ha reactions of aerobic energy production as the substrate of cytochrome oxidase (CCO) --the terminal exlzyme of the mitochondrial respiratory system. That is why oxygen deficiency under some conditions can limit or completely suppress aerobic energy production. The levels

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Section: Time Course Of Respiratory Dysfunction In Hypoxiamentioning

confidence: 99%

Bioenergetic hypoxia: Definition, mechanisms, and methods of correction

Luk’yanova

1997

Bull Exp Biol Med

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“…This is bound to activate enzymes for the subsequent reactions, ff so, then glutamate should be expected to influence primarily the level of succihate dehydrogenase (SDH). Indeed, as shown in several studies [1,3,5], glutamate has an activating effect on succinate oxidation, and such activation is usually explained by elimination of oxaloacetic acid, which inhibits SDH [1].The purpose of this study was to elucidate the possible reasons for alterations in the level of SDH in response to sensory stimulation of different types. …”

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confidence: 93%

“…Most of the glutamate is taken up by astrocytes [13]. The oxidation of exogenous glutamate provides an external energy source for astrocytes during neuronal excitation [5]. The remaining glutamate is taken up by neurons [13].…”

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confidence: 99%

Effect of sensory input on the levels of enzymes involved in energy metabolism

1994

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Presentation of sensory stimuli of various modalities to rats immediately before their decapitation led to a significant increase in the level of succmate dehydrogenase in the hippocampus, the magnitude of the increase being dependent on the number of stimuli presented. In each individual case, this enzyme's activity was proportional to the amplitude of the population spike recorded in the hippocampus of the same rat. An inverse relationship was noted between the rate of plastic processes in the hippocampus upon rhythmic stimulation and succinate dehydrogenase activity.Key Words: sensory stimulation; hippocampus; succinate dehydrogenase; population spike; frequency facilitationThe regulation of cell-cell interactions is inextricably bound up with assimilation-dissimilation processes. It has been shown that a major part of the glutamate secreted from nerve terminals becomes involved in energy metabolism [10][11][12]14,15]. Most of the glutamate is taken up by astrocytes [13]. The oxidation of exogenous glutamate provides an external energy source for astrocytes during neuronal excitation [5]. The remaining glutamate is taken up by neurons [13].These findings have enabled a hypothesis to be formulated concerning astro-neuronal interactions during functional activity.A convenient structure for verifying the validity of this hypothesis is the hippocampus. The main pathways in the latter are known to be glutamatergic [8]. Presentation of sensory stimuli should be accompartied by an elevation of glutamate secretion in the hippocampus and, according to the above hypothesis, will lead to increased uptake of glutamate by astrocytes followed by its entry into the Krebs cycle. This is bound to activate enzymes for the subsequent reactions, ff so, then glutamate should be expected to influence primarily the level of succihate dehydrogenase (SDH). Indeed, as shown in several studies [1,3,5], glutamate has an activating effect on succinate oxidation, and such activation is usually explained by elimination of oxaloacetic acid, which inhibits SDH [1].The purpose of this study was to elucidate the possible reasons for alterations in the level of SDH in response to sensory stimulation of different types. MATERIALS AND METHODSFour groups of Wistar rats were used for the experiments. Control rats were decapitated without being exposed to any stimulation. The second group were presented 15 light flashes immediately before decapitation, the third group was exposed to 15 electrocutaneous stimuli, and the fourth group,

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“…In contrast, HR to hypoxia animals have reduced excitability and anxiety, milder aggressiveness, more pronounced internal inhibition, low sensitivity to any provocative factors, and tendency to social domination. Acute hypoxia induces an inhibitory response in HR rats (Goryacheva et al, 1993 ; Livanova et al, 1992 ; Lukyanova, 1997 , 2005 ; Lukyanova et al, 2009c ).…”

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Mitochondria-controlled signaling mechanisms of brain protection in hypoxia

2015

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The article is focused on the role of the cell bioenergetic apparatus, mitochondria, involved in development of immediate and delayed molecular mechanisms for adaptation to hypoxic stress in brain cortex. Hypoxia induces reprogramming of respiratory chain function and switching from oxidation of NAD-related substrates (complex I) to succinate oxidation (complex II). Transient, reversible, compensatory activation of respiratory chain complex II is a major mechanism of immediate adaptation to hypoxia necessary for (1) succinate-related energy synthesis in the conditions of oxygen deficiency and formation of urgent resistance in the body; (2) succinate-related stabilization of HIF-1α and initiation of its transcriptional activity related with formation of long-term adaptation; (3) succinate-related activation of the succinate-specific receptor, GPR91. This mechanism participates in at least four critical regulatory functions: (1) sensor function related with changes in kinetic properties of complex I and complex II in response to a gradual decrease in ambient oxygen concentration; this function is designed for selection of the most efficient pathway for energy substrate oxidation in hypoxia; (2) compensatory function focused on formation of immediate adaptive responses to hypoxia and hypoxic resistance of the body; (3) transcriptional function focused on activated synthesis of HIF-1 and the genes providing long-term adaptation to low pO2; (4) receptor function, which reflects participation of mitochondria in the intercellular signaling system via the succinate-dependent receptor, GPR91. In all cases, the desired result is achieved by activation of the succinate-dependent oxidation pathway, which allows considering succinate as a signaling molecule. Patterns of mitochondria-controlled activation of GPR-91- and HIF-1-dependent reaction were considered, and a possibility of their participation in cellular-intercellular-systemic interactions in hypoxia and adaptation was proved.

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Respiration and oxidative phosphorylation of the mitochondria of the brain of rats with various types of behavior

Cited by 4 publications

References 4 publications

Bioenergetic hypoxia: Definition, mechanisms, and methods of correction

Bioenergetic hypoxia: Definition, mechanisms, and methods of correction

Effect of sensory input on the levels of enzymes involved in energy metabolism

Mitochondria-controlled signaling mechanisms of brain protection in hypoxia

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