Physical activity increases mRNA for brain-derived neurotrophic factor and nerve growth factor in rat brain

Neeper, Shawne A.; Gómez‐Pinilla, Fernando; Choi, Jor-Shan; Cotman, Carl W.

doi:10.1016/0006-8993(96)00273-9

Cited by 849 publications

(476 citation statements)

References 53 publications

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“…Previous works have showed that exercise regulates gene expression in the spinal cord [21][22][23][24]. The increased motor and sensory scores after exercise in the current study now demonstrates a direct functional outcome of exercise-dependent change.…”

Section: Discussionsupporting

confidence: 58%

Effect of Exercise Program on the Rehabilitation of Patients with Cervical Spondylotic Myelopathy

Kumar¹,

Lal²,

Dharmarajan³

2012

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Study Design: A clinical trial of 30 consecutive patients with cervical spondylotic myelopathy (CSM). Objectives: To evaluate the effect of directed physical exercise in patients with CSM and to measure severity of myelopathy before and after an exercise program. Setting: Christian Medical College and Hospital, India. Participants: Thirty patients with CSM (mean age = 54.1 years) with Nuricks Grade 2 and 3. Background: Myelopathy of the spinal cord can be caused by degenerative process of the cervical vertebrae and it is the most common type of dysfunction of the spinal cord in adult population. CSM usually develops insidiously and the natural history is not well understood, there is debate over the indication for operative vs non operative management. Method: Patients participated in a 6-week exercise program, consisting of active exercises to upper and lower extremities, scapulothoracic muscles, and gentle stretches, sub maximal isometric exercises of the deep neck flexors, relaxation and immobilization with a cervical hard collar. Main Outcome Measures: The mJOA (modified Japanese orthopaedic association score) and ASIA motor and sensory scoring. The results were processed by using Wilcoxon sign rank test. Results: After comparing the values at the beginning and end of the program a satisfactory neurological result (sensorimotor/motor and sensory) was obtained in all thirty patients. Conclusion: The exercise program had a positive impact for most of the variables of the study. Exercise intervention with neck immobilization may be a treatment of choice in early stages of CSM. Future randomized controlled studies would provide insight into the effectiveness and clinical relevance of this intervention.

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Section: Discussionsupporting

confidence: 58%

Effect of Exercise Program on the Rehabilitation of Patients with Cervical Spondylotic Myelopathy

Kumar¹,

Lal²,

Dharmarajan³

2012

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“…Via molecular techniques, it was systematically shown that exercise could up-regulate NT such as nerve growth factor (NGF) and brain derived nerve factor (BDNF) endogenously [6,7]. Such NT had been reported to facilitate recovery from brain injury such as stroke [8].…”

Section: Exercise and The Brainmentioning

confidence: 99%

Potential Therapeutic Effects of Exercise to the Brain

Ang

Gómez‐Pinilla²

2007

CMC

115

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Exercise is a well-recognized facet of modern living; however, the threat of sedentary lifestyle is ever increasing with the arrival of the technological period. Although the beneficial effects of exercise to the health and function of the brain have been accepted by the scientific and medical community, much remains to be achieved to understand its mechanisms of action. With the advent of modern investigative tools, several more key molecular and cellular players have been implicated in the above process. Such include the family of neurotrophins (e.g. NGF and BDNF) and their receptors, some pro-inflammatory cytokines (L-1beta, IL-6, TNF-alpha, IFN-gamma), microglia and astrocytes, and the cholinergic neuronal cells in the forebrain. While experiments based on the voluntary exercise paradigm has been the preferred approach to studying the brain, less is known about the forced paradigm. We will discuss in this review how molecular players may feature differently in the context of exercise and more importantly how their actions converged to impact the structure, and function (learning and memory) of the CNS.

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“…Historical studies have demonstrated the effects of exercise on the CNS that uses neurotransmitters and trophic factors involved in energy homeostasis, such as norepinephrine, γ-amino butyric acid, serotonin (5-HT; Dishman 1997), and brain-derived neurotrophic factor (BDNF; Neeper et al 1996). Furthermore, 40-day voluntary running wheel training significantly increases neuropeptide Y gene expression in Sprague-Dawley male rat ARC nucleus and DMH (Lewis et al 1993).…”

Section: Introductionmentioning

confidence: 99%

Voluntary exercise improves hypothalamic and metabolic function in obese mice

Laing¹,

Do²,

Matsubara³

et al. 2016

Journal of Endocrinology

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Exercise plays a critical role in regulating glucose homeostasis and body weight. However, the mechanism of exercise on metabolic functions associated with the CNS has not been fully understood. C57BL6 male mice (n = 45) were divided into three groups: normal chow diet, high-fat diet (HFD) treatment, and HFD along with voluntary running wheel exercise training for 12 weeks. Metabolic function was examined by the Comprehensive Lab Animal Monitoring System and magnetic resonance imaging; phenotypic analysis included measurements of body weight, food intake, glucose and insulin tolerance tests, as well as insulin and leptin sensitivity studies. By immunohistochemistry, the amount changes in the phosphorylation of signal transducer and activator of transcription 3, neuronal proliferative maker Ki67, apoptosis positive cells as well as pro-opiomelanocortin (POMC)-expressing neurons in the arcuate area of the hypothalamus was identified. We found that 12 weeks of voluntary exercise training partially reduced body weight gain and adiposity induced by an HFD. Insulin and leptin sensitivity were enhanced in the exercise training group verses the HFD group. Furthermore, the HFD-impaired POMC-expressing neuron is remarkably restored in the exercise training group. The restoration of POMC neuron number may be due to neuroprotective effects of exercise on POMC neurons, as evidenced by altered proliferation and apoptosis. In conclusion, our data suggest that voluntary exercise training improves metabolic symptoms induced by HFD, in part through protected POMC-expressing neuron from HFD and enhanced leptin signaling in the hypothalamus that regulates whole-body energy homeostasis. Exercise restores HFD-impaired POMC-expression neuronb t laing, k do and others

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Physical activity increases mRNA for brain-derived neurotrophic factor and nerve growth factor in rat brain

Cited by 849 publications

References 53 publications

Effect of Exercise Program on the Rehabilitation of Patients with Cervical Spondylotic Myelopathy

Effect of Exercise Program on the Rehabilitation of Patients with Cervical Spondylotic Myelopathy

Potential Therapeutic Effects of Exercise to the Brain

Voluntary exercise improves hypothalamic and metabolic function in obese mice

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