Negatively charged air ions are of interest of researchers and physicians as an effective means of prophylaxis and treatment of a wide range of diseases. Our previous studies showed that negatively charged air ions have normalizing effects on important physiological functions in rats subjected to prolonged chronic stress [3] and acute immobilization stress [4]. These studies used either long-lasting (three weeks) exposure to air ions during chronic induction of neurosis or pre-treatment (daily for one week) exposure before acute experiments in the immobilization stress model. It remained unclear whether short periods of exposure to air ions had prophylactic effects during the actual development of immobilization stress. Since the adaptational abilities of the body, especially resistance to stress-inducing factors, can depend on the type of nervous system [1, 2, 6], studies were performed with consideration of the typological characteristics of the animals' behavior. The aim of the present work was to study these points.Experiments were carried out using 64 male Wistar rats (250-350 g). All animals were kept in standard animal-house conditions with natural illumination. Air was ionized using an t~lion-132 device (an up-todate modification of the "Chizhevskii lamp" electroeffluvial air ionizer) for 1 h as animals were immobilized. The intensity of air ion formation was 31.6 ions/sec. Rats were placed 2 m from the air ionizer.llnstitute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, Moscow.
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,
Old rats are found to have greatly reduced capacities for learning conditioned responses of various types, particularly when induced to develop a neurosis-like state which impairs autonomic functions and their regulation. The development of hypertensive responses is accompanied at the cellular level by a significant rise of succinate dehydrogenase activity in the sensorimotor cortex of young neurotic rats and by its significant fall in that of their old counterparts, in which the predominant oxidation substrates are NAD-dependent compounds.
The study explores the effects of oxygen-nitrogen and oxygen-argon hypoxic mixtures (5-6%) on energy metabolism in rats. It is shown that in animals breathing an argoncontaining hypoxic mixture oxidative phosphorylation is less affected by acute hypoxia that in animals breathing a nitrogen-containing mixture. Key Words: hypoxia; argon; nitrogenInert gases under high barometric pressure exert a pronounced biological effect: an inert-gas narcosis. Moreover, inert gases under normal and elevated pressure are not biologically inert and modulate the rate of fundamental biological processes [2,8], in particular they enhance oxygen consumption by hepato-However, we found no publications on the effect of inert gases in hypoxic mixtures on respiratory enzymes.It has been previously demonstrated that life span of rats breathing hypoxic oxygen-argon mixture containing 4% oxygen 2-fold longer than that of rats breathing hypoxic nitrogen-oxygen mixture with the same percentage of oxygen.In the present study we investigated the effect of argon on the respiratory enzymes NADH dehydrogenase (NADH-DH) and succinate dehydrogenase (SDH) in the motor cortex under hypoxic conditions. MATERIALS AND METHODSRandom-bred albino rats were divided into 4 groups (4 rats per group) and placed to an air-conditioned The chamber was then ventilated with hypoxic (7% oxygen) oxygen-argon (group l) or oxygennitrogen (group 2) mixture until oxygen content decreased to 7% and then it was maintained within 5-6%. Group 3 animals breathed air (control). Temperature in the chanber was 19-20~ content of CO 2 did not exceeded 0.4 kPa. The duration of the experiment was 1 h. Group 4 animals were intact.All animals were decapitated immediately after the experiment, heads were wrapped in aluminum foil and frozen.Activity of respiratory enzymes SDH and NADH-DH in the motor cortex was measured using a quantitative histochemical method [5]. The amount of formazan (M) formed by 1 M protein nitrogen for 1 min at 37~ was taken as one unit of enzyme activity and expressed in milliunits (raM) formazan per 1 rain. Morphological evaluation of enzyme activity was carried out. RESULTSIn group 1, SDH and NADH-DH activities after inhalation of an oxygen-argon mixture decreased by 17% in comparison with intact rats (Fig. 1).In group 2, activities of both enzymes after inhalation of nitrogen-oxygen mixture decreased by 30%,
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