Physical exercise induces structural alterations in the hippocampal astrocytes: exploring the role of BDNF-TrkB signaling

Fahimi, Atoossa; Baktir, Mehmet; Moghadam, Sarah; Mojabi, Fatemeh S.; Sumanth, Krithika; McNerney, M. Windy; Ponnusamy, Ravikumar; Salehi, Ahmad

doi:10.1007/s00429-016-1308-8

Cited by 64 publications

(45 citation statements)

References 68 publications

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“…Many mechanisms are involved in such adaptation, exerting significant regulatory control over many facets of a neuronal function and leading to the biological effects of the hippocampus, including cognitive functioning and neurogenesis (Chou et al, 2018;Firth et al, 2018;Liu and Nusslock, 2018;Hill and Polk, 2019). A previous study has shown that treadmill exercise in mice increases BDNF expression by regulating BDNF mRNA and protein expression in the hippocampus (Fahimi et al, 2017). Similar changes were observed in the NT group in the present study.…”

Section: Discussionsupporting

confidence: 86%

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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Section: Discussionsupporting

confidence: 86%

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

Zheng

Yin

et al. 2020

Front. Mol. Neurosci.

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“…Under the influence of the training process, increased BDNF expression in the hippocampus, cerebral cortex, ST, brainstem, and spinal cord was observed [131,174,179,181,182]. Animal studies have shown that long-term endurance training increased both TrkB receptor and TH expression in structures involved in extrapyramidal movement regulation, i.e., in the ST and midbrain [128,129,179,[183][184][185]. As previously mentioned, the key element of neurotrophin-related neuroprotection is the IP3/Akt kinase pathway [186].…”

Section: Possible Mechanisms Underlying the Protective Effect Of Bndfmentioning

confidence: 87%

BDNF as a Promising Therapeutic Agent in Parkinson’s Disease

Pałasz

Wysocka

Gąsiorowska

et al. 2020

IJMS

341

197

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Brain-derived neurotrophic factor (BDNF) promotes neuroprotection and neuroregeneration. In animal models of Parkinson's disease (PD), BDNF enhances the survival of dopaminergic neurons, improves dopaminergic neurotransmission and motor performance. Pharmacological therapies of PD are symptom-targeting, and their effectiveness decreases with the progression of the disease; therefore, new therapeutical approaches are needed. Since, in both PD patients and animal PD models, decreased level of BDNF was found in the nigrostriatal pathway, it has been hypothesized that BDNF may serve as a therapeutic agent. Direct delivery of exogenous BDNF into the patient's brain did not relieve the symptoms of disease, nor did attempts to enhance BDNF expression with gene therapy. Physical training was neuroprotective in animal models of PD. This effect is mediated, at least partly, by BDNF. Animal studies revealed that physical activity increases BDNF and tropomyosin receptor kinase B (TrkB) expression, leading to inhibition of neurodegeneration through induction of transcription factors and expression of genes related to neuronal proliferation, survival, and inflammatory response. This review focuses on the evidence that increasing BDNF level due to gene modulation or physical exercise has a neuroprotective effect and could be considered as adjunctive therapy in PD.

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“…In addition, following spinal cord injury, TrkB.T1 knockout astrocytes have slower migration/proliferation in response to BDNF and downregulated migration and proliferation pathways (Matyas et al, 2017). Interestingly, BDNF, TrkB, and astrocytic territory are all increased by exercise (Fahimi et al, 2017), which enhances cognition (Gomez-Pinilla and Hillman, 2013).…”

Section: Discussionmentioning

confidence: 99%

Visualizing BDNF cell-to-cell transfer reveals astrocytes are the primary recipient of neuronal BDNF

Stahlberg

Kügler

Dean

2018

Preprint

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Brain-derived neurotrophic factor (BDNF) is essential for neuronal growth, differentiation, and synaptic plasticity. Although the release and effects of BDNF have been well-studied separately, the transfer of BDNF between cells has not been investigated. Using a fourfluorophore imaging approach to identify both the cell of origin and target cells, we quantified transfer of BDNF. Surprisingly, we found that astrocytes are the main recipient of neuronally expressed BDNF. We further found that astrocytes specifically take up mature (and not pro) BDNF released by neurons. Over-expression of TrkB in neurons redirects released BDNF from astrocytes to neurons, indicating that TrkB level determines neuronal versus astrocytic BDNF uptake. Increased neuronal activity further increased astrocytic (but not neuronal) uptake of neuronally expressed BDNF. Finally, we demonstrate that astrocytes are not simply a sink for excess BDNF, but that BDNF taken up by astrocytes mediates physiological effects on the astrocytic population by increasing astrocytic territory.

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Physical exercise induces structural alterations in the hippocampal astrocytes: exploring the role of BDNF-TrkB signaling

Cited by 64 publications

References 68 publications

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

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

BDNF as a Promising Therapeutic Agent in Parkinson’s Disease

Visualizing BDNF cell-to-cell transfer reveals astrocytes are the primary recipient of neuronal BDNF

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