Treadmill exercise induces age and protocol-dependent epigenetic changes in prefrontal cortex of Wistar rats

2016 ◽  
Vol 313 ◽  
pp. 82-87 ◽  
Author(s):  
Laura Reck Cechinel ◽  
Carla Giovana Basso ◽  
Karine Bertoldi ◽  
Bruna Schallenberger ◽  
Louisiana Carolina Ferreira de Meireles ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Wistar Rats ◽  
Treadmill Exercise ◽  
Epigenetic Changes

scholarly journals Exercise Ameliorates Spinal Cord Injury by Changing DNA Methylation

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 143
Author(s):  
Ganchimeg Davaa ◽  
Jin Young Hong ◽  
Tae Uk Kim ◽  
Seong Jae Lee ◽  
Seo Young Kim ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Motor Cortex ◽  
Functional Recovery ◽  
Treadmill Exercise ◽  
Exercise Group ◽  
Control Group ◽  
Epigenetic Changes ◽  
Cord Injury ◽  
The Brain

Exercise training is a traditional method to maximize remaining function in patients with spinal cord injury (SCI), but the exact mechanism by which exercise promotes recovery after SCI has not been identified; whether exercise truly has a beneficial effect on SCI also remains unclear. Previously, we showed that epigenetic changes in the brain motor cortex occur after SCI and that a treatment leading to epigenetic modulation effectively promotes functional recovery after SCI. We aimed to determine how exercise induces functional improvement in rats subjected to SCI and whether epigenetic changes are engaged in the effects of exercise. A spinal cord contusion model was established in rats, which were then subjected to treadmill exercise for 12 weeks. We found that the size of the lesion cavity and the number of macrophages were decreased more in the exercise group than in the control group after 12 weeks of injury. Immunofluorescence and DNA dot blot analysis revealed that levels of 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) in the brain motor cortex were increased after exercise. Accordingly, the expression of ten-eleven translocation (Tet) family members (Tet1, Tet2, and Tet3) in the brain motor cortex also elevated. However, no macrophage polarization was induced by exercise. Locomotor function, including Basso, Beattie, and Bresnahan (BBB) and ladder scores, also improved in the exercise group compared to the control group. We concluded that treadmill exercise facilitates functional recovery in rats with SCI, and mechanistically epigenetic changes in the brain motor cortex may contribute to exercise-induced improvements.

scholarly journals Increased lactate threshold after five weeks of treadmill aerobic training in rats

2014 ◽  
Vol 74 (2) ◽  
pp. 444-449 ◽  
Author(s):  
WH. Brito Vieira ◽  
MJE. Halsberghe ◽  
MLB. Schwantes ◽  
SEA. Perez ◽  
V. Baldissera ◽  
...  
Keyword(s):  
Lactate Threshold ◽  
Wistar Rats ◽  
Aerobic Training ◽  
Treadmill Exercise ◽  
Training Programme ◽  
Control Group ◽  
Sedentary Control ◽  
Running Speed ◽  
Treadmill Exercise Test ◽  
Physiological Adaptations

The aim of the present study was to analyse the lactate threshold (LT) changes in rats submitted to an aerobic treadmill-training programme. Twenty-five Wistar rats were divided into two groups: a sedentary control group (CG), and a trained group (TG) submitted to an aerobic training during 5 weeks. All the animals were submitted to an incremental treadmill exercise test in order to determine LT. There was an increase in the maximum running speed in the TG (from 32.25 ± 1.27 to 47.75 ± 3.13 m.min–1 – p = 0.001), and running speed at LT (from 26.21 ± 1.15 to 35.30 ± 2.24 m.min–1 – p = 0.004), a part from the reduction in blood lactate at LT. LT can be determined in rats, and aerobic training induced positive oxidative physiological adaptations in the animals.

The role of prefrontal cortex dopamine D2 and D3 receptors in the mechanism of action of venlafaxine and deep brain stimulation in animal models of treatment-responsive and treatment-resistant depression

2019 ◽  
Vol 33 (6) ◽  
pp. 748-756 ◽  
Author(s):  
Mariusz Papp ◽  
Piotr Gruca ◽  
Magdalena Lason ◽  
Monika Niemczyk ◽  
Paul Willner
Keyword(s):  
Prefrontal Cortex ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Memory Consolidation ◽  
Wistar Rats ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto ◽  
Deep Brain

Aims: The Wistar-Kyoto rat has been validated as an animal model of treatment-resistant depression. Here we investigated a role of dopamine D2 and D3 receptors in the ventro-medial prefrontal cortex in the mechanism of action of deep brain stimulation in Wistar-Kyoto rats and venlafaxine in Wistar rats. Methods: Wistar or Wistar-Kyoto rats were exposed chronically to chronic mild stress. Wistar rats were treated chronically with venlafaxine (10 mg/kg) beginning after two weeks of chronic mild stress; Wistar-Kyoto rats received two sessions of deep brain stimulation before behavioural tests. L-742,626 (1 µg), a D2 receptor agonist, or 7-OH DPAT (3 µg), a D3 receptor antagonist, were infused into the ventro-medial prefrontal cortex immediately following the exposure trial in the Novel Object Recognition Test, and discrimination between novel and familiar object was tested one hour later. Results: Chronic mild stress decreased sucrose intake and impaired memory consolidation; these effects were reversed by venlafaxine in Wistar rats and deep brain stimulation in Wistar-Kyoto rats. In control animals, L-742,626 and 7-OH DPAT also impaired memory consolidation. In Wistar rats, venlafaxine reversed the effect of L-742,626 in controls, but not in the chronic mild stress group, and venlafaxine did not reverse the effect of 7-OH DPAT in either group. In Wistar-Kyoto rats, deep brain stimulation reversed the effect of both L-742,626 and 7-OH DPAT in both control and chronic mild stress groups. Conclusions: We conclude that the action of venlafaxine to reverse the impairment of memory consolidation caused by chronic mild stress in Wistar rats involves D2 receptors in the ventro-medial prefrontal cortex; but the effect of deep brain stimulation to reverse the same effect in Wistar-Kyoto rats does not.

Extracellular dopamine levels are lower in the medial prefrontal cortex of alcohol-preferring rats compared to Wistar rats

Alcohol ◽  
2006 ◽  
Vol 38 (1) ◽  
pp. 5-12 ◽  
Author(s):  
Eric A. Engleman ◽  
Cynthia M. Ingraham ◽  
William J. McBride ◽  
Lawrence Lumeng ◽  
James M. Murphy
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Wistar Rats ◽  
Extracellular Dopamine

scholarly journals Effect of Electronic Cigarette on Brain Prefrontal Cortex of Male Wistar Rats

2020 ◽  
Vol 6 (3) ◽  
pp. 98-102
Author(s):  
Centaury Noor Kuncorowati ◽  
◽  
Sofia Mawaddatul Urfah ◽  
Devanico Yuangga Duta Maulana ◽  
Mochamad Bahrudin ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Wistar Rats ◽  
Electronic Cigarette ◽  
Male Wistar Rats

scholarly journals Long-term epigenetic changes in offspring mice exposed to alcohol during gestation and lactation

2019 ◽  
Vol 33 (12) ◽  
pp. 1562-1572 ◽  
Author(s):  
Lídia Cantacorps ◽  
Silvia Alfonso-Loeches ◽  
Consuelo Guerri ◽  
Olga Valverde
Keyword(s):  
Prefrontal Cortex ◽  
Alcohol Drinking ◽  
Alcohol Exposure ◽  
Learning Task ◽  
Spectrum Disorder ◽  
Epigenetic Changes ◽  
Histone H4 ◽  
Spectrum Disorders ◽  
Foetal Alcohol Spectrum Disorders

Background: Alcohol exposure impairs brain development and leads to a range of behavioural and cognitive dysfunctions, termed as foetal alcohol spectrum disorders. Although different mechanisms have been proposed to participate in foetal alcohol spectrum disorders, the molecular insights of such effects are still uncertain. Using a mouse model of foetal alcohol spectrum disorder, we have previously shown that maternal binge-like alcohol drinking causes persistent effects on motor, cognitive and emotional-related behaviours associated with neuroimmune dysfunctions. Aims: In this study, we sought to evaluate whether the long-term behavioural alterations found in offspring with early exposure to alcohol are associated with epigenetic changes in the hippocampus and prefrontal cortex. Methods: Pregnant C57BL/6 female mice underwent a model procedure for binge alcohol drinking throughout both the gestation and lactation periods. Subsequently, adult offspring were assessed for their cognitive function in a reversal learning task and brain areas were extracted for epigenetic analyses. Results: The results demonstrated that early binge alcohol exposure induces long-term behavioural effects along with alterations in histone acetylation (histone H4 lysine 5 and histone H4 lysine 12) in the hippocampus and prefrontal cortex. The epigenetic effects were linked with an imbalance in histone acetyltransferase activity that was found to be increased in the prefrontal cortex of mice exposed to alcohol. Conclusions: In conclusion, our results reveal that maternal binge-like alcohol consumption induces persistent epigenetic modifications, effects that might be associated with the long-term cognitive and behavioural impairments observed in foetal alcohol spectrum disorder models.

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