Effects of Treadmill Exercise Combined with MK 801 Treatment on Neuroblast Differentiation in the Dentate Gyrus in Rats

Choi, Jung Hoon; Yoo, Ki‐Yeon; Lee, Choong Hyun; Yi, Sun Shin; Yoo, Dae Young; Seong, Je Kyung; Yoon, Yeo Sung; Hwang, In Koo; Won, Moo‐Ho

doi:10.1007/s10571-010-9619-4

Cited by 13 publications

(7 citation statements)

References 45 publications

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“…Circulatory IGF1 or VEGF have also been reported as essential factors in exercise-induced AHN [ 31 – 33 ]. Other factors, such as progranulin [ 34 ], steroids (glucocorticoid [ 35 ]), morphogens (Wnt [ 36 ]) and neurotransmitters (glutamate [ 37 ], neuropeptide Y [ 38 ] and beta-endorphin [ 39 ]), have also been assumed to be involved in these adaptations. Collectively, this evidence suggests that exercise promotes AHN through a complex regulatory mechanism, and numerous factors, including androgen, are potentially involved in ME-induced AHN.…”

Section: Introductionmentioning

confidence: 99%

Long-Term Mild, rather than Intense, Exercise Enhances Adult Hippocampal Neurogenesis and Greatly Changes the Transcriptomic Profile of the Hippocampus

et al. 2015

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Our six-week treadmill running training (forced exercise) model has revealed that mild exercise (ME) with an intensity below the lactate threshold (LT) is sufficient to enhance spatial memory, while intense exercise (IE) above the LT negates such benefits. To help understand the unrevealed neuronal and signaling/molecular mechanisms of the intensity-dependent cognitive change, in this rat model, we here investigated plasma corticosterone concentration as a marker of stress, adult hippocampal neurogenesis (AHN) as a potential contributor to this ME-induced spatial memory, and comprehensively delineated the hippocampal transcriptomic profile using a whole-genome DNA microarray analysis approach through comparison with IE. Results showed that only IE had the higher corticosterone concentration than control, and that the less intense exercise (ME) is better suited to improve AHN, especially in regards to the survival and maturation of newborn neurons. DNA microarray analysis using a 4 × 44 K Agilent chip revealed that ME regulated more genes than did IE (ME: 604 genes, IE: 415 genes), and only 41 genes were modified with both exercise intensities. The identified molecular components did not comprise well-known factors related to exercise-induced AHN, such as brain-derived neurotrophic factor. Rather, network analysis of the data using Ingenuity Pathway Analysis algorithms revealed that the ME-influenced genes were principally related to lipid metabolism, protein synthesis and inflammatory response, which are recognized as associated with AHN. In contrast, IE-influenced genes linked to excessive inflammatory immune response, which is a negative regulator of hippocampal neuroadaptation, were identified. Collectively, these results in a treadmill running model demonstrate that long-term ME, but not of IE, with minimizing running stress, has beneficial effects on increasing AHN, and provides an ME-specific gene inventory containing some potential regulators of this positive regulation. This evidence might serve in further elucidating the mechanism behind ME-induced cognitive gain.

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Section: Introductionmentioning

confidence: 99%

Long-Term Mild, rather than Intense, Exercise Enhances Adult Hippocampal Neurogenesis and Greatly Changes the Transcriptomic Profile of the Hippocampus

et al. 2015

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“…1 Experimental protocol for different groups, the days on which memory acquisition or retrieval were tested. Co control group, Ex-Re exercise-rest (withdrawal exercise) group, Re-Ex rest-exercise (exercised group) group, Ex-Ex exerciseexercise (continual exercise) group likelihood of receiving shock was controlled by exposing the sham-exercised group to the treadmill apparatus without switching on the treadmill at the start of the experiment (Uda et al 2006;Alaei et al 2008;Chen et al 2008;Reisi et al 2009;Choi et al 2011). These rats received the same electric shock when they stepped onto the grid.…”

Section: Exercise Paradigmsmentioning

confidence: 99%

Effect of forced exercise and exercise withdrawal on memory, serum and hippocampal corticosterone levels in rats

et al. 2015

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Evidence suggests that there are positive effects of exercise on learning and memory. Moreover, some studies have demonstrated that forced exercise plays the role of a stressor. This study was aimed at investigating the effects of different timing of exercise and exercise withdrawal on memory, and serum and hippocampal corticosterone (CORT) levels. Wistar rats were randomly divided into five groups: control, sham, exercise-rest (exercise withdrawal), rest-exercise (exercised group), and exercise-exercise (continuous exercise). Rats were forced to run on a treadmill for 1 h/day at a speed 20-21-m/min. Memory function was evaluated by the passive avoidance test in different intervals (1, 7 and 21 days) after foot shock. Findings showed that after the exercise withdrawal, short-term and mid-term memories, had significant enhancement compared to the control group, while the long-term memory did not present this result. In addition, the serum and hippocampal CORT levels were at the basal levels after the rest period in the exercise-rest group. In the rest-exercise group, exercise improved mid- and long-term memories, whereas continuous exercise improved all types short-, mid- and long-term memories, particularly the mid-term memory. Twenty-one and forty-two days of exercise significantly decreased the serum and hippocampal CORT levels. It seems that exercise for at least 21 days with no rest could affect biochemical factors in the brain. Also, regular continuous exercise plays an important role in memory function. Hence, the duration and withdraw of exercise are important factors for the neurobiological aspects of the memory responses.

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“…Increasing numbers of chemicals have recently been shown to affect the proliferation and differentiation of progenitor cells in the SGZ during postnatal life in mice and rats (Choi et al, 2011;Yoo et al, 2011). We have previously shown sustained fluctuations in the numbers of interneurons producing reelin or expressing calcium-binding proteins such as calretinin (Calb2) and parvalbumin (Pvalb) in the hilus of the dentate gyrus of rats after exposure to neurotoxic substances.…”

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confidence: 99%

Glycidol Induces Axonopathy by Adult-Stage Exposure and Aberration of Hippocampal Neurogenesis Affecting Late-Stage Differentiation by Developmental Exposure in Rats

Akane

Shiraki

Imatanaka

et al. 2013

Toxicological Sciences

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To investigate the neurotoxicity profile of glycidol and its effect on developmental hippocampal neurogenesis, pregnant Sprague Dawley rats were given drinking water containing 0, 100, 300, or 1000 ppm glycidol from gestational day 6 until weaning on day 21 after delivery. At 1000 ppm, dams showed progressively worsening gait abnormalities, and histopathological examination showed generation of neurofilament-L(+) spheroids in the cerebellar granule layer and dorsal funiculus of the medulla oblongata, central chromatolysis in the trigeminal nerve ganglion cells, and axonal degeneration in the sciatic nerves. Decreased dihydropyrimidinase-like 3(+) immature granule cells in the subgranular zone (SGZ) and increased immature reelin(+) or calbindin-2(+) γ-aminobutyric acid-ergic interneurons and neuron-specific nuclear protein (NeuN)(+) mature neurons were found in the dentate hilus of the offspring of the 1000 ppm group on weaning. Hilar changes remained until postnatal day 77, with the increases in reelin(+) and NeuN(+) cells being present at ≥ 300 ppm, although the SGZ change disappeared. Thus, glycidol caused axon injury in the central and peripheral nervous systems of adult rats, suggesting that glycidol targets the newly generating nerve terminals of immature granule cells, resulting in the suppression of late-stage hippocampal neurogenesis. The sustained hilar changes may be a sign of continued aberrations in neurogenesis and migration. The no-observed-adverse-effect level was determined to be 300 ppm (48.8mg/kg body weight/day) for dams and 100 ppm (18.5mg/kg body weight/day) for offspring. The sustained developmental exposure effect on offspring neurogenesis was more sensitive than the adult axonal injury.

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Effects of Treadmill Exercise Combined with MK 801 Treatment on Neuroblast Differentiation in the Dentate Gyrus in Rats

Cited by 13 publications

References 45 publications

Long-Term Mild, rather than Intense, Exercise Enhances Adult Hippocampal Neurogenesis and Greatly Changes the Transcriptomic Profile of the Hippocampus

Long-Term Mild, rather than Intense, Exercise Enhances Adult Hippocampal Neurogenesis and Greatly Changes the Transcriptomic Profile of the Hippocampus

Effect of forced exercise and exercise withdrawal on memory, serum and hippocampal corticosterone levels in rats

Glycidol Induces Axonopathy by Adult-Stage Exposure and Aberration of Hippocampal Neurogenesis Affecting Late-Stage Differentiation by Developmental Exposure in Rats

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