Hypoactivity Affects IGF-1 Level and PI3K/AKT Signaling Pathway in Cerebral Structures Implied in Motor Control

Mysoet, Julien; Canu, Marie‐Hélène; Cieniewski-Bernard, Caroline; Bastide, Bruno; Dupont, Erwan

doi:10.1371/journal.pone.0107631

Cited by 16 publications

(14 citation statements)

References 48 publications

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“…Sample sizes were determined based on a power analysis (power = 0.8, a = 0.05) using effect sizes observed in previous study (Mysoet et al 2014) as well as our pilot study. All quantitative results were presented as box-plot (box: first and third quartiles and median; whiskers: minimum and maximum).…”

Section: Discussionmentioning

confidence: 99%

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Synaptic protein changes after a chronic period of sensorimotor perturbation in adult rats: a potential role of phosphorylation/O‐GlcNAcylation interplay

Fourneau

Canu

Cieniewski-Bernard

et al. 2018

Journal of Neurochemistry

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In human, a chronic sensorimotor perturbation (SMP) through prolonged body immobilization alters motor task performance through a combination of peripheral and central factors. Studies performed on a rat model of SMP have shown biomolecular changes and a reorganization of sensorimotor cortex through events such as morphological modifications of dendritic spines (number, length, functionality). However, underlying mechanisms are still unclear. It is well known that phosphorylation regulates a wide field of synaptic activity leading to neuroplasticity. Another post‐translational modification that interplays with phosphorylation is O‐GlcNAcylation. This atypical glycosylation, reversible, and dynamic, is involved in essential cellular and physiological processes such as synaptic activity, neuronal morphogenesis, learning, and memory. We examined potential roles of phosphorylation/O‐GlcNAcylation interplay in synaptic plasticity within rat sensorimotor cortex after a SMP period. For this purpose, sensorimotor cortex synaptosomes were separated by sucrose gradient, in order to isolate a subcellular compartment enriched in proteins involved in synaptic functions. A period of SMP induced plastic changes at the pre‐ and post‐synaptic levels, characterized by a reduction in phosphorylation (synapsin1, α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazoleproprionic acid receptors (AMPAR) GluA2) and expression (synaptophysin, PSD‐95, AMPAR GluA2) of synaptic proteins, as well as a decrease in MAPK/ERK42 activation. Expression levels of O‐GlcNAc transferase/O‐GlcNAcase enzymes was unchanged but we observed a specific reduction of synapsin1 O‐GlcNAcylation in sensorimotor cortex synaptosomes. The synergistic regulation of synapsin1 phosphorylation/O‐GlcNAcylation could affect pre‐synaptic neurotransmitter release. Associated with other pre‐ and post‐synaptic changes, synaptic efficacy could be impaired in somatosensory cortex of SMP rat. Thus, phosphorylation/O‐GlcNAcylation interplay appears to be involved in synaptic plasticity by finely regulating neural activity.

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Section: Discussionmentioning

confidence: 99%

“….] (Dupont et al 2011;Mysoet et al 2014). Despite these data, molecular and dynamic events associated with this synaptic plasticity, especially after SMP, remain to be clarified.…”

mentioning

confidence: 99%

Synaptic protein changes after a chronic period of sensorimotor perturbation in adult rats: a potential role of phosphorylation/O‐GlcNAcylation interplay

Fourneau

Canu

Cieniewski-Bernard

et al. 2018

Journal of Neurochemistry

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“…An alternative sensory deprivation model is that of hindlimb unloading (HU). In adult rats, 14 days of HU decreases IGF1 levels in the somatosensory cortex (Mysoet et al, 2014 ) and shrinks the somatotopic representation of the hindpaw. Administration of IGF1 prevents this change in somatotopic representation (Papadakis et al, 1996 ; Mysoet et al, 2015 ).…”

Section: Igf1 and The Adult Brain: Prolonged Survival Reduced Cell Dmentioning

confidence: 99%

Insulin-Like Growth Factor 1: At the Crossroads of Brain Development and Aging

Wrigley

Arafa

Tropea

2017

Front. Cell. Neurosci.

190

131

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Insulin-like growth factor 1 (IGF1) is a polypeptide hormone structurally similar to insulin. It is central to the somatotropic axis, acting downstream of growth hormone (GH). It activates both the mitogen-activated protein (MAP) kinase and PI3K signaling pathways, acting in almost every tissue in the body to promote tissue growth and maturation through upregulation of anabolic processes. Overall GH and IGF1 signaling falls with age, suggesting that it is this reduced IGF1 activity that leads to age-related changes in organisms. However, mutations that reduce IGF1-signaling activity can dramatically extend the lifespan of organisms. Therefore, the role of IGF1 in the overall aging process is unclear. This review article will focus on the role of IGF1 in brain development and aging. The evidence points towards a role for IGF1 in neurodevelopment both prenatally and in the early post-natal period, and in plasticity and remodeling throughout life. This review article will then discuss the hallmarks of aging and cognitive decline associated with falls in IGF1 levels towards the end of life. Finally, the role of IGF1 will be discussed within the context of both neuropsychiatric disorders caused by impaired development of the nervous system, and neurodegenerative disorders associated with aging. IGF1 and its derivatives are shown to improve the symptoms of certain neuropsychiatric disorders caused by deranged neurodevelopment and these effects have been correlated with changes in the underlying biology in both in vitro and in vivo studies. On the other hand, studies looking at IGF1 in neurodegenerative diseases have been conflicting, supporting both a role for increased and decreased IGF1 signaling in the underlying pathogenesis of these diseases.

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“…Our previous experience with HU mice, which were used for the present and other studies (Brocca et al, 2010 ; Desaphy et al, 2010 ; Maffei et al, 2014 ; Cannavino et al, 2015 ), indicates that HU can produced significant stress in about 6% of cases and during the first 3 days of suspension (Kawano et al, 1994 ; Morey-Holton and Globus, 2002 ; Basco et al, 2010 ; Gaignier et al, 2014 ; Mysoet et al, 2014 ), after which the levels of stress, serum, and urine corticosterone measured, returned to the normal ones of the non-suspended animals. Indeed, it had already been demonstrated (Kawano et al, 1994 ) that in 5-week-old rats corticosterone urinary excretion in the control group was 87.4 ± 12.8 ng/day and did not change throughout the unloading time.…”

Section: Discussionmentioning

confidence: 66%

Reduction of Movement in Neurological Diseases: Effects on Neural Stem Cells Characteristics

et al. 2018

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Both astronauts and patients affected by chronic movement-limiting pathologies face impairment in muscle and/or brain performance. Increased patient survival expectations and the expected longer stays in space by astronauts may result in prolonged motor deprivation and consequent pathological effects. Severe movement limitation can influence not only the motor and metabolic systems but also the nervous system, altering neurogenesis and the interaction between motoneurons and muscle cells. Little information is yet available about the effect of prolonged muscle disuse on neural stem cells characteristics. Our in vitro study aims to fill this gap by focusing on the biological and molecular properties of neural stem cells (NSCs). Our analysis shows that NSCs derived from the SVZ of HU mice had shown a reduced proliferation capability and an altered cell cycle. Furthermore, NSCs obtained from HU animals present an incomplete differentiation/maturation. The overall results support the existence of a link between reduction of exercise and muscle disuse and metabolism in the brain and thus represent valuable new information that could clarify how circumstances such as the absence of load and the lack of movement that occurs in people with some neurological diseases, may affect the properties of NSCs and contribute to the negative manifestations of these conditions.

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Hypoactivity Affects IGF-1 Level and PI3K/AKT Signaling Pathway in Cerebral Structures Implied in Motor Control

Cited by 16 publications

References 48 publications

Synaptic protein changes after a chronic period of sensorimotor perturbation in adult rats: a potential role of phosphorylation/O‐GlcNAcylation interplay

Synaptic protein changes after a chronic period of sensorimotor perturbation in adult rats: a potential role of phosphorylation/O‐GlcNAcylation interplay

Insulin-Like Growth Factor 1: At the Crossroads of Brain Development and Aging

Reduction of Movement in Neurological Diseases: Effects on Neural Stem Cells Characteristics

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