On the Run for Hippocampal Plasticity

Cooper, C'iana P.; Moon, Hyo Youl; Praag, Henriette van

doi:10.1101/cshperspect.a029736

Cited by 119 publications

(81 citation statements)

References 468 publications

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“…Evidence from human and animal studies has established that regular aerobic exercise can improve cognitive performance and can protect against anxiety and depression 18,19 . Cognitive challenges performed during exercise result in levels of enhancement of synaptic plasticity, as well as learning and memory, greater than either challenge alone 20 .…”

Section: Neuronal Adaptations To Imsmentioning

confidence: 99%

Intermittent metabolic switching, neuroplasticity and brain health

et al. 2018

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During evolution, individuals whose brains and bodies functioned well in a fasted state were successful in acquiring food, enabling their survival and reproduction. With fasting and extended exercise, liver glycogen stores are depleted and ketones are produced from adipose-cell-derived fatty acids. This metabolic switch in cellular fuel source is accompanied by cellular and molecular adaptations of neural networks in the brain that enhance their functionality and bolster their resistance to stress, injury and disease. Here, we consider how intermittent metabolic switching, repeating cycles of a metabolic challenge that induces ketosis (fasting and/or exercise) followed by a recovery period (eating, resting and sleeping), may optimize brain function and resilience throughout the lifespan, with a focus on the neuronal circuits involved in cognition and mood. Such metabolic switching impacts multiple signalling pathways that promote neuroplasticity and resistance of the brain to injury and disease.

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Section: Neuronal Adaptations To Imsmentioning

confidence: 99%

Intermittent metabolic switching, neuroplasticity and brain health

et al. 2018

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“…The p75 is a member of the TNF receptor superfamily that can bind to BDNF and transmits signals important for determining which neurons survive during development (Huang and Reichardt, 2001). At present, the precise molecular mechanisms regarding exercisemediated neurogenesis are still not fully known (Baptista and Andrade, 2018;Cooper et al, 2018). Importantly, BDNF is a candidate mechanism underlying these exercise-induced benefits that help optimize brain plasticity outcomes via exercise intervention (Baptista and Andrade, 2018;Cooper et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…At present, the precise molecular mechanisms regarding exercisemediated neurogenesis are still not fully known (Baptista and Andrade, 2018;Cooper et al, 2018). Importantly, BDNF is a candidate mechanism underlying these exercise-induced benefits that help optimize brain plasticity outcomes via exercise intervention (Baptista and Andrade, 2018;Cooper et al, 2018). Acute high-intensity exercise increases the expression of BDNF (Venezia et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Excessive Treadmill Training Enhances Brain-Specific MicroRNA-34a in the Mouse Hippocampus

Zheng

Yin

et al. 2020

Front. Mol. Neurosci.

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Background: An imbalance between total training load and total recovery may cause overtraining (OT). The purpose of the present study was to verify the effects of OT on the expression of brain-derived neurotrophic factor (BDNF), its receptor tropomyosin receptor kinase B (TrkB) and p75 and the dynamic expression patterns of brainspecific miR-34a and miR-124 or inflammation-related miR-21 and miR-132 in the mouse hippocampus.Method: Eight weeks old C57BL/6J mice were randomly assigned to the control (CON), normal training (NT) and OT groups. An 8-week OT training protocol was applied to evaluate the phenotype of mice endurance (incremental load test, ILT) and cognitive capacity (Morris water maze test). We used qRT-PCR and immunoblotting to detect changes in the molecular level of hippocampal samples.Result: Compared with the CON, both NT and OT decreased bodyweight after 8-week training. After 8-week of training, NT increased the exhaustion velocity (EV) while the EV of OT was lower than NT. Mice in NT decreased the escape latency than CON. The percentage of time spent in the probe quadrant and the number of crossing platform times in NT were higher than CON and OT. The BDNF, p75 and TrkB mRNA levels were increased in NT than CON, only the p75 mRNA was increased in OT. The NT exhibited increased protein levels of BDNF and TrkB compared to CON. The protein expression of BDNF was decreased in OT than NT and CON. The protein level of p75 in the OT was higher than in NT and CON. In addition, the phosphorylation level of TrkB in OT was higher than CON and NT. Only the miR-34a level was increased in the OT. Moreover, the expression of miR-34a was found to be negatively correlated with the expression of BDNF, and the increase in miR-34a level was accompanied by a decrease in performance.Frontiers in Molecular Neuroscience | www.frontiersin.org January 2020 | Volume 13 | Article 7 Xu et al. Brain-Specific MicroRNA-34a and Excessive TrainingConclusion: In summary, the training-evoked increase in the BDNF level may help to improve performance, whereas this conditioning is lost after OT. Moreover, miR-34a potentially mediated changes in the expression of BDNF and may reflect the decrease in performance after OT.

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“…Physical activity is generally considered beneficial for brain health and cognitive function in normal subjects. Exercising implicates positive effects for the nervous tissue, such as increased blood flow, increased synapse plasticity and increased neurogenesis, particularly in the hippocampus (Cooper et al, 2018). Several studies have shown that exercise promotes the recovery of the hippocampal function after various forms of neural insult (Kim et al, 2011;Cechetti et al, 2012;Winocur et al, 2014;Klein et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Moderate exercise prevents the cell atrophy caused by hypothyroidism in rats

Martínez-Salazar¹,

Villanueva²,

Pacheco-Rosado³

et al. 2020

Acta Neurobiologiae Experimentalis

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Adult-onset hypothyroidism is associated with an increase in cell atrophy of the hippocampal pyramidal neurons. Physical exercise implies diverse actions on the neural tissue that promote neuron proliferation and survival. The beneficial effects of exercise seem to be inversely linked to its intensity, so that strenuous exercise has reduced protective effects. In this study we evaluated the capacity of a moderate forced-exercise routine to counteract the neurodegenerative effects of a hypothyroid condition induced during adulthood.Simultaneously with a chronic anti-thyroid chemical treatment, a group of rats was forced to walk in a motorized wheel for 30 min daily five times a week. In four weeks of treatment the rats developed a plain hypothyroid condition that in non-exercised rats was accompanied by a marked increase in the number of atrophic cells in all CA regions of the hippocampus. The forced-exercise treatment did not counter the development of hypothyroidism and its signs, but it did prevent almost completely the associated neuronal damage in all CA regions. The forced exercise also improved the cognitive function in a spatial-learning test. These results indicate that moderate exercise has the potential to prevent the structural and functional deficits associated with a hypothyroid condition.

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On the Run for Hippocampal Plasticity

Cited by 119 publications

References 468 publications

Intermittent metabolic switching, neuroplasticity and brain health

Intermittent metabolic switching, neuroplasticity and brain health

Excessive Treadmill Training Enhances Brain-Specific MicroRNA-34a in the Mouse Hippocampus

Moderate exercise prevents the cell atrophy caused by hypothyroidism in rats

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