Brain energy metabolism is increased by chronic administration of bupropion

2012 ◽  
Vol 24 (2) ◽  
pp. 115-121 ◽  
Author(s):  
Gabriela K. Ferreira ◽  
Gislaine T. Rezin ◽  
Mariane R. Cardoso ◽  
Cinara L. Gonçalves ◽  
Lislaine S. Borges ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Malate Dehydrogenase ◽  
Respiratory Chain ◽  
Citrate Synthase ◽  
Chronic Administration ◽  
Mitochondrial Respiratory Chain ◽  
Brain Energy Metabolism ◽  
Respiratory Chain Complexes ◽  
Chain Complexes ◽  
Brain Energy

Objectives: Based on the hypothesis that energy impairment may be involved in the pathophysiology of depression, we evaluated the activities of citrate synthase, malate dehydrogenase, succinate dehydrogenase (SDH), mitochondrial respiratory chain complexes I, II, II-III, IV and creatine kinase (CK) in the brain of rats submitted to chronic administration of bupropion.Methods: Animals received daily administration of bupropion dissolved in saline (10 mg/kg, intraperitoneal) at 1.0 ml/kg body weight. The rats received injections once a day for 14 days; control rats received an equivalent volume of saline. Twelve hours after the last administration, the rats were killed by decapitation and brain was rapidly removed and kept on an ice plate. The activities of the enzymes were measured in different brain areas.Results: We observed that the activities of citrate synthase and malate dehydrogenase, mithocondrial respiratory chain complexes I, II-III and IV and CK were not altered after chronic administration of bupropion. However, SDH activity was increased in the prefrontal cortex and cerebellum. In the hippocampus, cerebellum and striatum the activity of complex II was increased after chronic administration of bupropion.Conclusions: Our results demonstrated that bupropion increased some enzymes of brain energy metabolism. These findings are in accordance with other studies which showed that some antidepressants may improve energy metabolism. The present results reinforce the hypothesis that antidepressants modulate brain energy metabolism.

Activity of mitochondrial respiratory chain is increased by chronic administration of antidepressants

2011 ◽  
Vol 23 (3) ◽  
pp. 112-118 ◽  
Author(s):  
Giselli Scaini ◽  
Débora D. Maggi ◽  
Bruna T. De-Nês ◽  
Cinara L. Gonçalves ◽  
Gabriela K. Ferreira ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Prefrontal Cortex ◽  
Energy Metabolism ◽  
Respiratory Chain ◽  
Chronic Administration ◽  
Mitochondrial Respiratory Chain ◽  
Brain Energy Metabolism ◽  
Complex Iv ◽  
Complex Ii ◽  
Brain Energy

Objective: Depressive disorders, including major depression, are serious and disabling for affected patients. Although the neurobiological understanding of major depressive disorder focuses mainly on the monoamine hypothesis, the exact pathophysiology of depression is not fully understood.Methods: Animals received daily intra-peritoneal injections of paroxetine (10 mg/kg), nortriptyline (15 mg/kg) or venlafaxine (10 mg/kg) in 1.0 ml/kg volume for 15 days. Twelve hours after the last injection, the rats were killed by decapitation, where the brain was removed and homogenised. The activities of mitochondrial respiratory chain complexes in different brain structures were measured.Results: We first verified that chronic administration of paroxetine increased complex I activity in prefrontal cortex, hippocampus, striatum and cerebral cortex. In addition, complex II activity was increased by the same drug in hippocampus, striatum and cerebral cortex and complex IV activity in prefrontal cortex. Furthermore, chronic administration of nortriptyline increased complex II activity in hippocampus and striatum and complex IV activity in prefrontal cortex, striatum and cerebral cortex. Finally, chronic administration of venlafaxine increased complex II activity in hippocampus, striatum and cerebral cortex and complex IV activity in prefrontal cortex.Conclusion: On the basis of the present findings, it is tempting to speculate that an increase in brain energy metabolism by the antidepressant paroxetine, nortriptyline and venlafaxine could play a role in the mechanism of action of these drugs. These data corroborate with other studies suggesting that some antidepressants modulate brain energy metabolism.

Effects of maintenance electroshock on mitochondrial respiratory chain and creatine kinase activities in the rat brain

2012 ◽  
Vol 24 (5) ◽  
pp. 275-285
Author(s):  
Gislaine Z. Réus ◽  
Roberto B. Stringari ◽  
Gislaine T. Rezin ◽  
Daiana P. Pezente ◽  
Giselli Scaini ◽  
...  
Keyword(s):  
Creatine Kinase ◽  
Energy Metabolism ◽  
Rat Brain ◽  
Respiratory Chain ◽  
Brain Area ◽  
Mitochondrial Respiratory Chain ◽  
Respiratory Chain Complexes ◽  
Chain Complexes ◽  
Male Wistar Rats ◽  
Mitochondrial Respiratory

Réus GZ, Stringari RB, Rezin GT, Pezente DP, Scaini G, Maggi DD, De-Nês BT, Streck EL, Quevedo J, Feier G. Effects of maintenance electroshock on mitochondrial respiratory chain and creatine kinase activities in the rat brain.Objective: Electroconvulsive therapy is used efficacious treatment for a variety of complicated psychiatric disorders and evidences have indicated that energy metabolism impairment may be involved in pathophysiology and treatment of mood disorders. This work was performed to determine creatine kinase and mitochondrial respiratory chain activities at different times after the maintenance electroconvulsive shock (ECS).Methods: Male Wistar rats received a protocol mimicking therapeutic of maintenance or simulated ECS (sham) and were subsequently sacrificed immediately after, 48 h and 7 days after the last maintenance ECS. We measured creatine kinase and mitochondrial respiratory chain activities in the prefrontal cortex, hippocampus, cortex, cerebellum and striatum.Results: Our results showed that maintenance ECS alter respiratory chain complexes and creatine kinase activities in the rat brain, but these effects were related to brain area and time after the ECS, in which the animal were killed.Conclusion: Finally, these findings further support the hypothesis that alteration on the energy metabolism could be involved in the therapeutic or adverse effects of ECS.

scholarly journals Activity of Mitochondrial Respiratory Chain Enzymes after Transient Focal Ischemia in the Rat

1997 ◽  
Vol 17 (11) ◽  
pp. 1166-1169 ◽  
Author(s):  
Laura Canevari ◽  
Satoshi Kuroda ◽  
Timothy E. Bates ◽  
John B. Clark ◽  
Bo K. Siesjö
Keyword(s):  
Respiratory Chain ◽  
Citrate Synthase ◽  
Mitochondrial Respiratory Chain ◽  
Artery Occlusion ◽  
Respiratory Chain Complexes ◽  
Secondary Damage ◽  
Chain Complexes ◽  
Postischemic Recirculation ◽  
Transient Focal Ischemia ◽  
Mitochondrial Respiratory

Previous results demonstrated that after 2-hour middle cerebral artery occlusion (MCAO) in the rat, 1- to 2-hour recirculation temporarily restored the bioenergetic state and mitochondrial function, but secondary deterioration took place after 4 hours. The authors measured the activity of mitochondrial respiratory chain complexes, citrate synthase, and glutamate dehydrogenase as possible targets of secondary damage. Focal and penumbral tissues were sampled in the control condition, after 2 hours of MCAO, and after 1, 2, or 4 hours of postischemic recirculation; two groups were treated with α-phenyl-N- tert-butyl-nitrone (PBN). Complex IV activity transiently decreased after MCAO, but after recirculation all measured activities returned to control values.

scholarly journals 4- hydroxy-3,5-di-tret-butyl cinnamic acid restores the activity of the hippocampal mitochondria in rats under permanent focal cerebral ischemia

2021 ◽  
Author(s):  
Dmitry Pozdnyakov
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Middle Cerebral Artery ◽  
Respiratory Chain ◽  
Cinnamic Acid ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Mitochondrial Respiratory Chain ◽  
Respiratory Chain Complexes ◽  
Chain Complexes

Background and Purpose: Ischemic stroke remains one of the leading causes of death in the population. In addition, mitochondrial dysfunction is an essential part of the pathogenesis of cerebral ischemia and is a promising pharmacotherapeutic target. Experimental Approach: the work was performed on male Wistar rats, which were simulated cerebral ischemia by irreversible occlusion of the middle cerebral artery. 4-hydroxy-3,5-di-tret-butyl cinnamic acid (25 mg/kg, 50 mg/kg and 100 mg/kg) was injected intraperitoneally for 3 days after ischemia (daily). On the 4th day of the experiment, the changes of rat’s cognitive functions in the Morris water maze test, cellular respiration processes, the activity of the mitochondrial respiratory chain complexes and citrate synthase activity, the intensity of oxidative stress and apoptosis reactions were assessed. Key Results: it was found that the administration of 4-hydroxy-3,5-di-tret-butyl cinnamic acid at doses of 25 mg/kg and 50 mg/kg practically equivalently promotes the restoration of aerobic metabolism reactions and the activity of the mitochondrial respiratory chain complexes, decrease of the intensity of oxidative stress reactions and apoptosis, as well as an increase in the activity of citrate synthase. As a result, the restoration of mitochondrial function in the hippocampal cells contributed to the restoration of the animal’s spatial memory. Conclusion and Implications: a study showed that 4-hydroxy-3,5-di-tret-butyl cinnamic acid at doses of 25 mg/kg and 50 mg/kg has a neuroprotective effect on hippocampal neurons under conditions of permanent occlusion of the middle cerebral artery, realized by restoration of mitochondrial function.

Physiological diversity of mitochondrial oxidative phosphorylation

2006 ◽  
Vol 291 (6) ◽  
pp. C1172-C1182 ◽  
Author(s):  
G. Benard ◽  
B. Faustin ◽  
E. Passerieux ◽  
A. Galinier ◽  
C. Rocher ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Respiratory Chain ◽  
Citrate Synthase ◽  
Intrinsic Activity ◽  
Mitochondrial Oxidative Phosphorylation ◽  
Respiratory Chain Complexes ◽  
Mitochondrial Content ◽  
Physiological Diversity ◽  
Chain Complexes ◽  
Functional Features

To investigate the physiological diversity in the regulation and control of mitochondrial oxidative phosphorylation, we determined the composition and functional features of the respiratory chain in muscle, heart, liver, kidney, and brain. First, we observed important variations in mitochondrial content and infrastructure via electron micrographs of the different tissue sections. Analyses of respiratory chain enzyme content by Western blot also showed large differences between tissues, in good correlation with the expression level of mitochondrial transcription factor A and the activity of citrate synthase. On the isolated mitochondria, we observed a conserved molar ratio between the respiratory chain complexes and a variable stoichiometry for coenzyme Q and cytochrome c, with typical values of [1–1.5]:[30–135]:[3]:[9–35]:[6.5–7.5] for complex II:coenzyme Q:complex III:cytochrome c:complex IV in the different tissues. The functional analysis revealed important differences in maximal velocities of respiratory chain complexes, with higher values in heart. However, calculation of the catalytic constants showed that brain contained the more active enzyme complexes. Hence, our study demonstrates that, in tissues, oxidative phosphorylation capacity is highly variable and diverse, as determined by different combinations of 1) the mitochondrial content, 2) the amount of respiratory chain complexes, and 3) their intrinsic activity. In all tissues, there was a large excess of enzyme capacity and intermediate substrate concentration, compared with what is required for state 3 respiration. To conclude, we submitted our data to a principal component analysis that revealed three groups of tissues: muscle and heart, brain, and liver and kidney.

Sign in / Sign up

Export Citation Format

Share Document