Brain Tissue Respiration Research Articles

Carnosic Acid Improves Outcome after Repetitive Mild Traumatic Brain Injury.

In the majority of cases, the cognitive and behavioral impairments resulting from a mild traumatic brain injury (TBI) (also referred to as concussion) wane within days to weeks. In contrast, these impairments can persist for months to years after repetitive mild TBI (rmTBI). The cellular and molecular mechanisms underlying these impairments are not well understood. In the present study, we examined the consequences of rmTBI (three weight drops each separated by 72 h) on brain tissue respiration, pathology, and cognitive performance in mice. The transcription factor nuclear factor-erythroid 2-realted factor 2 (Nrf2) has been demonstrated to enhance the expression of numerous cytoprotective genes. Carnosic acid (CA) has been shown to activate Nrf2 and suppress the proinflammatory transcription factor nuclear factor kappa B (NF-κB). Because contemporaneous activation of cytoprotective genes and inhibition of proinflammatory genes can be beneficial, we questioned whether CA can be used to mitigate the pathobiology of rmTBI. The rmTBI increased hippocampal adenosine triphosphate-linked tissue respiration and proton leak that were unaffected by CA treatment. The rmTBI also caused significant motor and cognitive dysfunction, as tested using the foot fault, Barnes maze, and novel object recognition tasks. These impairments occurred in the absence of visible neuronal or dendritic loss. Post-rmTBI administration of CA significantly improved motor and cognitive function, and decreased Gfap and Iba1 immunoreactivities within white matter tracks. Taken together, these results show that rmTBI can cause cognitive impairments in the absence of overt neuronal pathologies, and post-injury treatment with CA can lessen some of these impairments.

Kernicterus: Past, Present, and Future

The concept of a relationship between severe neonatal hyperbilirubinemia and kernicterus evolved slowly. Jaundice was recognized in ancient as well as biblical times as a manifestation of disease. However, according to Louis K. Diamond (Fig. 1), who reviewed the history of neonatal jaundice, (1) the first record concerning jaundice of the newborn appears to be by Barthomomaeus Metlinger in 1473 in his book Ein Regiment der Jungen Kinder . The occurrence of jaundice shortly after birth as well as some suggestions for homeopathic treatment were mentioned by Michael Ettmuller in his 1708 treatise “De Infantum Morbis.” (1) An early description of icterus neonatorum was published in 1742 in London by John Burton in his treatise “A Full View of All the Diseases Incident to Children.” He suggested that “jaundice generally yields to any gentle purgative.” (1) This same approach was used by Condie in 1853 in Philadelphia. (2) At that time, he wrote that icterus neonatorum seemed to be “connected with the want of a free evacuation of meconium.” He suggested the use of castor oil or a small measure of calomel or rhubarb. It is interesting that he noted that the jaundice was known at times to be accompanied by a “good deal of drowsiness.” There were several publications in France concerning neonatal jaundice in the late eighteenth and early nineteenth centuries, the most significant of which, according to Thor Hansen, (3) was the thesis submitted by Jacques Francois Hervieux and defended by him for his M.D. degree at the University of Paris in 1847. The thesis was entitled “De l’ictere des nouveau-nes” (On the jaundice of newborns). Thor Hansen, to whom we are grateful for having reviewed the original French thesis, pointed out that the introductory section of the Hervieux thesis contains a valuable review of works by …

Antidepressants and brain respiration.

Imipramine and clorgyline, at concentrations of 0.002 M, inhibit the respiration of brain tissue by 82 and 71 per cent respectively, while chloropromazine and tranylcypromine, at concentrations of 0.01 M, inhibit it about 25 per cent. Deprenyl and amphetamine at a concentration of 0.002 M inhibit brain tissue respiration by 12 and 18 per cent respectively. Respiration in brain is least affected by lithium chloride (only 5 per cent inhibition).

Drug-induced alterations in respiration of rat brain cortex and striatum slices in a carbon dioxide-bicarbonate-buffered medium

Rates of oxygen utilization were measured with an oxygen electrode in rat brain cortex and striatum slices. Values obtained for respiratory rates in cortex (approximately 85 μmoles/hr/g wet weight) and striatum (about 43 μmoles/hr/g) were similar in both bicarbonate and tris-buffered solutions. Addition of potassium chloride (to 70 mM) elicited an increase in oxygen utilization in both preparations. Exposure to procaine (10 mM) reduced the respiration rate to levels substantially below control values and prevented the K +-induced increase in respiration rate. Pentobarbital sodium (1 mM) and, perhaps to a lesser extent, caffeine (5 mM) also decreased the control respiration rates and inhibited the K +-induced stimulation of respiration rates. Nicotine (0.67 mM) had no effect on control or K +-stimulated respiration rates in cortex or striatum slices. Effects of procaine appeared to be additive with those of caffeine and pentobarbital, and are probably attained by different cellular mechanisms. Observation of similar respiratory rates in bicarbonate and tris solutions also suggests that correlations may be attempted between brain tissue respiration studies in CO 2-free media and measurements of ionic parameters in the presence of bicarbonate-buffered solutions.

The effects of sera from psychiatric patients on guinea pig brain tissue respiration.

The in vitro effect of human sera on tissue respiration has been studied. Blood specimens from hospitalized patients and “normal” controls were added to fresh minced guinea pig brain respiring in glucose and normal Ringer solutions. With the use of a Warburg apparatus, oxidative activity of the brain tissue was assessed by measuring O2 uptake. The results indicate that serum of both hospitalized schizophrenics and nonschizo-phrenic psychiatric patients have an inhibitory effect on guinea pig brain tissue respiration as compared with normal control sera. Whatever the factor responsible, it is statistically significant and does not appear to effect the availability of glucose to the cell, since comparable findings are seen with the use of glucose-free Ringer. The findings suggest that hospitalization or its effects may be producing various biochemical changes interpreted by others as pathogenetic for schizophrenia and reemphasize the need for adequately selected control groups in psychobiological research. The results and observations are discussed and related to those of previous authors working in this area.

Temperature acclimation in the central nervous system of rainbow trout ( Salmo gairdnerii)

1. 1. The midbrain response to direct electrical stimulation of the retina was measured in rainbow trout acclimated to 10°C and following transfer and acclimation to 4 and 16°C. The evoked midbrain potential consisted first of a positive deflection upon which was superimposed two negative spikes of supposed pre-synaptic origin, and secondly of a slow negative potential, interpreted as post-synaptic in origin. 2. 2. Transfer of 10° acclimated trout to 4° caused an average 39 per cent protraction of the entire midbrain response pattern. After 21 days' acclimation to 4°, the negative spike latencies had decreased to 18 and 19 per cent above the 10° controls and the duration of the slow potential had decreased to 16 per cent above the 10° controls. 3. 3. Transfer of 10° acclimated trout to 16° caused an initial shortening of the negative spike latencies and slow potential duration. These values lengthened somewhat during acclimation to 16° but, since a similar lengthening occurred int he 10° controls, the change was judged noncompensatory. 4. 4. Thus, significant compensation occurred in response to low temperature acclimation (4°) but not to high temperature acclimation (16°). These results contrast with brain tissue respiration measurements that show that metabolic compensation is much more complete between 10 and 16° than between 4 and 10°.

CEREBRAL CORTICAL OXYGEN UPTAKE STIMULATING FACTOR FROM CEREBRAL CORTICAL SLICES.

SummaryIncubation of rat cortical slices for 2 hours in a non-substrated phosphate saline medium at room temperature, produces an “activating” medium which is capable of stimulating the oxygen uptake of freshly cut cortical slices when subsequently determined in it. The nature of the activating material is unknown. The presence of glucose (11.5 mm/l) or glucose plus additional substrates (Krebs III medium(4)) in the incubation medium masks the stimulation. Neither an increase in the temperature of incubation to 37.34°C, possibly allowing more “activating” material to diffuse into the medium, nor the presence of calcium in the incubation medium which would partially inhibit the respiration of brain tissue was sufficient to allow a stimulation to be observed in the presence of added substrates.

Effects of chlorpromazine on brain tissue respiration.

This work demonstrates that there is a biphasic effect on brain tissue respiration with respect to time interval after chlorpromazine administration to an intact animal. The first phase, lasting about 16 hours in the rat, reflects an inhibition of respiratory activity while the second, persisting about 4 days, reflects an enhancement of respiration. It is not clear at this point whether this biphasic effect is due to a peculiarity of metabolic activity or simply represents a different rate of penetration into cortical and subcortical structures. We have demonstrated that chlorpromazine can induce opposite effects on brain tissue respiration in different parts of the brain. The hemispheres including the cerebellum show an increased respiration while the midbrain and stem show a depression of respiration following chlorpromazine administration.

Adaptation to ethanol in rats with special reference to brain tissue respiration

Adaptation to ethanol in rats with special reference to brain tissue respiration

Effects of acetylcholine analogues and ethanol on the respiration of brain cortex tissue in vitro

Unstimulated and electrically stimulated brain cortex slices were exposed to compounds related to acetylcnoline, and to Triton, with or without 1.96 × 10 −1 M (0.9 per cent) ethanol. The lipid-insoluble substances acetylcholine, curare, deca- and suxa-methonium were inactive on the brain tissue respiration. In unstimulated tissue, the lipid-soluble acetylcholine analogues pyridine-2-aldoximedodecyl iodide (PAD) and cetyltrimethyl-ammonium bromide (Cetavlon), like ethanol, caused a transient increase in respiration. Cetavlon, cetylpyridine chloride (CPC) and Triton reduced the respiration of both stir ulated and unstimulated tissue at approximately identical concentrations, the relative effect on unstimulated tissue being smaller. 10 −4 M PAD and 1.8 × 10 −3 M atrepine abolished the response to stimulation almost completely leaving unstimulated tissue unaffected. Ethanol significantly increased the effect of atropine, PAD, Cetavlon and CPC on stimulated tissue. The non-ionized detergent Triton was not synergistic with ethanol. In intact rats, PAD potentiated ethanol action on the CNS Cetavlon acted similarly, but caused strong haemolysis when injected with ethanol. In vitro, haemolysis caused by Cetavlon was not increased by low ethanol concentrations. The results are consistent with the hypothesis that the acetylcholine system is involved in the reaction of brain slices to electrical stimulation, and indicate that ethanol may depress the functional response to stimulation by unspecific action on this system.

Effect of age, sex and gonadal hormone on brain tissue respiration of albino rats

Effects of age, sex and female gonadal hormone on brain respiration in rats are studied. Oxygen consumption of the entire brain of rat rises as the weight of animal increases. It is maximum when the body weight reaches about 150 gm. Then there is a decrease in oxygen consumption. Female sex hormone seems to have an inhibitory action on the brain respiration.

薬物の中枢興奮作用とアミンオキシダーゼ活性及び脳組織呼吸に及ぼす影響について

Relationship between awakening effect and inhibitory action of amine-oxidase activity of a drug, discovered by Mann, Quastel, and Ohta, was examined systematically by the use of analeptics, such as methylpropamin, dimethylpropamin, and 2-(3, 4-methylene-dioxyphenyl) isopropylamine, and a series of other pharmaceuticals. Further examinations were made on the possibility of the use of this point as a supplementary means in the judgement of potency of awakening effect, which is difficult to be obtained from animal tests. At the same time, effect of these pharmaceutics on brain tissue respiration was tested with a rabbit. Majority of these pharmaceutics indicated inhibitory action on amine-oxidase activity in greater or lesser degree and the levorotatory compound of analeptics, which does not indicate awakening effect in human body, inhibited amine-oxidase activity, same as dextrorotatory compound. It was found that the correlationship between awakening effect and inhibition of amine-oxidase activity was exceptionally weak. At the same time, these pharmaceutics indicated weak inhibitory action on tissue respiration but there seemed to be no correlation between that and awakening effect.

Inhibitory effect of citrinin (C13H1405) on the dehydrogenase system of rat's kidney, liver and brain tissue, specially concerning the mechanism of polyuria observed in the poisoned animal.

The inhibitory effect of citrinin, one of the quinoid compounds, on the respiration and succinic dehydrogenase activity of the kidney, liver and brain tissue of normal rats, and the depression of the respiration and succinic dehydrogenase activity of the kidney tissue, but no effect on the respiration of brain tissue in the poisoned rats were investigated. The probable relation between the inhibition of tubular reabsorption of water and the depressed activity of dehydrogenase of the kidney tissue was discussed.

大黒鼠脳組織呼吸の活性化エネルギー

大黒鼠脳組織呼吸の活性化エネルギー

大黒鼠脳組織呼吸の活性化エネルギー

大黒鼠脳組織呼吸の活性化エネルギー

Lysergic Acid Diethylamide (Lsd-25): Xxiii. Comparative Effects of Lsd-25 and Related Ergot Drugs on Brain Tissue Respiration and on Human Behavior

Lysergic Acid Diethylamide (Lsd-25): Xxiii. Comparative Effects of Lsd-25 and Related Ergot Drugs on Brain Tissue Respiration and on Human Behavior

Inhibitory effect of malonate on the respiration of brain tissue, with special reference to the potassium effect.

IT has long been known that, in brain cortex slices, both aerobic glycolysis and respiration are enhanced markedly when potassium chloride (0.1 M) is added to the suspension medium1, this metabolic effect of potassium being peculiar to nervous tissue2 and abolished by grinding the material3. In view of the manner in which the increased aerobic glycolysis and respiration respond to various metabolic poisons such as potassium cyanide, malonate and monoiodoacetate, it seems possible that the type of linkage of these two metabolic routes differs from that under normal conditions4.