Exercise affects glutamate receptors in postsynaptic densities from cortical mice brain

Dietrich, Marcelo O.; Mantese, Carlos Eduardo Aliatti; Porciúncula, Lisiane O.; Ghisleni, Gabriele; Vinadé, Lúcia; Souza, Diogo O.; Portela, Luis Valmor

doi:10.1016/j.brainres.2005.09.038

Cited by 75 publications

(53 citation statements)

References 53 publications

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“…It was identified that exercise is a necessary step for initiating activity of the NMDA receptor in the hippocampus (42) and that exercise-enhanced NMDA receptor expression promotes postnatal motor-unit maturation in a spinal muscular atrophy mouse model (43). Treadmill exercise increases NMDA receptor immunoreactivity and protein level in the hippocampus (44).…”

Section: Discussionmentioning

confidence: 99%

Voluntary wheel running ameliorates symptoms of MK-801-induced schizophrenia in mice

Kim

Kang

Park

et al. 2014

Molecular Medicine Reports

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Abstract. Schizophrenia is a chronic and severe mental disorder characterized by the disintegration of cognitive thought processes and emotional responses. Despite the precise cause of schizophrenia remains unclear, it is hypothesized that a dysregulation of the N-methyl-D-aspartate (NMDA) receptor in the brain is a major contributing factor to its development. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family and is implicated in learning and memory processes. In the present study, we investigated in vivo the effects of voluntary wheel running on behavioral symptoms associated with NMDA receptor expression, using MK-801-induced schizophrenic mice. Abilify (aripiprazole), a drug used to treat human schizophrenia patients, was used as the positive control. For the assessment of behavioral symptoms affecting locomotion, social interaction and spatial working memory, the open-field, social interaction and Morris water maze tests were conducted. For investigating the biochemical parameters, NMDA receptor expression in the hippocampal CA2-3 regions and prefrontal cortex was detected by NMDA immunofluorescence and BDNF expression in the hippocampus was measured using western blot analysis. MK-801 injection for 14 days induced schizophrenia-like behavioral abnormalities with decreased expression of the NMDA receptor and BDNF in the brains of mice. The results indicated that free access to voluntary wheel running for 2 weeks alleviated schizophrenia-like behavioral abnormalities and increased the expression of NMDA receptor and BDNF, comparable to the effects of aripiprazole treatment. In the present study, the results suggest that NMDA receptor hypofunctioning induced schizophrenia-like behaviors, and that voluntary wheel running was effective in reducing these symptoms by increasing NMDA receptor and BDNF expression, resulting in an improvement of disease related behavioral deficits.

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Section: Discussionmentioning

confidence: 99%

Voluntary wheel running ameliorates symptoms of MK-801-induced schizophrenia in mice

Kim

Kang

Park

et al. 2014

Molecular Medicine Reports

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“…However, reports in the literature suggest a role for neurotrophic factors, such as brain-derived neurotrophic factor, fibroblast growth factor, or glial-derived neurotrophic factor, which through activation of down-stream pathways, such as protein kinases, may influence synaptic plasticity and terminal neurotransmission (Gomez-Pinilla et al, 1997Cohen et al, 2003). The glutamatergic corticostriatal pathway may be another candidate system involved in exercise-related alterations in dopamine release, because it is known to be an important modulator of dopamine release in the striatum, and our previous work has shown alterations in the density of striatal glutamate immunolabeling in the MPTP plus exercise mice compared with sedentary MPTP-lesioned mice Fisher et al, 2004;Dietrich et al, 2005). Overall, these results indicate that the recovery of motor behavior can in fact occur through novel compensatory mechanisms within the basal ganglia and that the mechanisms of this recovery may be different in the lesioned compared with the nonlesioned basal ganglia.…”

Section: Figurementioning

confidence: 99%

Effects of Treadmill Exercise on Dopaminergic Transmission in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Lesioned Mouse Model of Basal Ganglia Injury

Petzinger¹,

Walsh²,

Akopian³

et al. 2007

J. Neurosci.

299

239

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Studies have suggested that there are beneficial effects of exercise in patients with Parkinson's disease, but the underlying molecular mechanisms responsible for these effects are poorly understood. Studies in rodent models provide a means to examine the effects of exercise on dopaminergic neurotransmission. Using intensive treadmill exercise, we determined changes in striatal dopamine in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse. C57BL/6J mice were divided into four groups: (1) saline, (2) saline plus exercise, (3) MPTP, and (4) MPTP plus exercise. Exercise was started 5 d after MPTP lesioning and continued for 28 d. Treadmill running improved motor velocity in both exercise groups. All exercised animals also showed increased latency to fall (improved balance) using the accelerating rotarod compared with nonexercised mice. Using HPLC, we found no difference in striatal dopamine tissue levels between MPTP plus exercise compared with MPTP mice. There was an increase detected in saline plus exercise mice. Analyses using fast-scan cyclic voltammetry showed increased stimulus-evoked release and a decrease in decay of dopamine in the dorsal striatum of MPTP plus exercise mice only. Immunohistochemical staining analysis of striatal tyrosine hydroxylase and dopamine transporter proteins showed decreased expression in MPTP plus exercise mice compared with MPTP mice. There were no differences in mRNA transcript expression in midbrain dopaminergic neurons between these two groups. However, there was diminished transcript expression in saline plus exercise compared with saline mice. Our findings suggest that the benefits of treadmill exercise on motor performance may be accompanied by changes in dopaminergic neurotransmission that are different in the injured (MPTP-lesioned) compared with the noninjured (saline) nigrostriatal system.

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“…Increasing evidence indicates that physical exercise induces adaptations at the cellular, molecular, and systemic levels that positively affect the health of the brain (Dietrich et al, 2005;Droste et al, 2006;Stranahan et al, 2009). These effects include an increase in synaptic plasticity and peripheral sensitivity to insulin as well as a slowing of age-related cognitive decline and a delay in the onset of neurodegenerative diseases.…”

Section: Introductionmentioning

confidence: 99%

Exercise increases insulin signaling in the hippocampus: Physiological effects and pharmacological impact of intracerebroventricular insulin administration in mice

et al. 2010

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Increasing evidence indicates that physical exercise induces adaptations at the cellular, molecular, and systemic levels that positively affect the brain. Insulin plays important functional roles within the brain that are mediated by insulin‐receptor (IR) signaling. In the hippocampus, insulin improves synaptic plasticity, memory formation, and learning via direct modulation of GABAergic and glutamatergic receptors. Separately, physical exercise and central insulin administration exert relevant roles in cognitive function. We here use CF1 mice to investigate (i) the effects of voluntary exercise on hippocampal insulin signaling and memory performance and (ii) whether central insulin administration alters the effects of exercise on hippocampal insulin signaling and memory performance. Adult mice performed 30 days of voluntary exercise on running wheel and afterward both, sedentary and exercised groups, received intracerebroventricular (icv) injection of saline or insulin (0.5–5 mU). Memory performance was assessed using the inhibitory avoidance and water maze tasks. Hippocampal tissue was measured for [U‐14C] glucose oxidation and the immunocontent of insulin receptor/signaling (IR, pTyr, pAktser473). Additionally, the phosphorylation of the glutamate NMDA receptor NR2B subunit and the capacity of glutamate uptake were measured, and immunohistochemistry was used to determine glial reactivity. Exercise significantly increased insulin peripheral sensitivity, spatial learning, and hippocampal IR/pTyrIR/pAktser473 immunocontent. Glucose oxidation, glutamate uptake, and astrocyte number also increased relative to the sedentary group. In both memory tasks, 5 mU icv insulin produced amnesia but only in exercised animals. This amnesia was associated a rapid (15 min) and persistent (24 h) increase in hippocampal pNR2B immunocontent that paralleled the increase in glial reactivity. In conclusion, physical exercise thus increased hippocampal insulin signaling and improved water maze performance. Overstimulation of insulin signaling in exercised animals, however, via icv administration impaired behavioral performance. This effect was likely the result of aberrant phosphorylation of the NR2B subunit. © 2010 Wiley‐Liss, Inc.

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Exercise affects glutamate receptors in postsynaptic densities from cortical mice brain

Cited by 75 publications

References 53 publications

Voluntary wheel running ameliorates symptoms of MK-801-induced schizophrenia in mice

Voluntary wheel running ameliorates symptoms of MK-801-induced schizophrenia in mice

Effects of Treadmill Exercise on Dopaminergic Transmission in the 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine-Lesioned Mouse Model of Basal Ganglia Injury

Exercise increases insulin signaling in the hippocampus: Physiological effects and pharmacological impact of intracerebroventricular insulin administration in mice

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