title: Hypoactivity affects IGF-1 level and PI3K/AKT signaling pathway in cerebral structures implied in motor control.
abstract: A chronic reduction in neuromuscular activity through prolonged body immobilization in human alters motor task performance through a combination of peripheral and central factors. Studies performed in a rat model of sensorimotor restriction have shown functional and biochemical changes in sensorimotor cortex. However, the underlying mechanisms are still unclear. Interest was turned towards a possible implication of Insulin-like Growth Factor 1 (IGF-1), a growth factor known to mediate neuronal excitability and synaptic plasticity by inducing phosphorylation cascades which include the PI3K-AKT pathway. In order to better understand the influence of IGF-1 in cortical plasticity in rats submitted to a sensorimotor restriction, we analyzed the effect of hindlimb unloading on IGF-1 and its main molecular pathway in structures implied in motor control (sensorimotor cortex, striatum, cerebellum). IGF-1 level was determined by ELISA, and phosphorylation of its receptor and proteins of the PI3K-AKT pathway by immunoblot. In the sensorimotor cortex, our results indicate that HU induces a decrease in IGF-1 level; this alteration is associated to a decrease in activation of PI3K-AKT pathway. The same effect was observed in the striatum, although to a lower extent. No variation was noticed in the cerebellum. These results suggest that IGF-1 might contribute to cortical and striatal plasticity induced by a chronic sensorimotor restriction.
authors.affiliation: Université Lille Nord de France, Lille, France; « Physical Activity, Muscle and Health » laboratory, EA 4488, IFR 114, Université Lille 1, Sciences et Technologies, Villeneuve d'Ascq, France.
authors.forename: Julien
authors.initials: J
authors.lastname: Mysoet
authors.affiliation: Université Lille Nord de France, Lille, France; « Physical Activity, Muscle and Health » laboratory, EA 4488, IFR 114, Université Lille 1, Sciences et Technologies, Villeneuve d'Ascq, France.
authors.forename: Marie-Hélène
authors.initials: MH
authors.lastname: Canu
authors.affiliation: Université Lille Nord de France, Lille, France; « Physical Activity, Muscle and Health » laboratory, EA 4488, IFR 114, Université Lille 1, Sciences et Technologies, Villeneuve d'Ascq, France.
authors.forename: Caroline
authors.initials: C
authors.lastname: Cieniewski-Bernard
authors.affiliation: Université Lille Nord de France, Lille, France; « Physical Activity, Muscle and Health » laboratory, EA 4488, IFR 114, Université Lille 1, Sciences et Technologies, Villeneuve d'Ascq, France.
authors.forename: Bruno
authors.initials: B
authors.lastname: Bastide
authors.affiliation: Université Lille Nord de France, Lille, France; « Physical Activity, Muscle and Health » laboratory, EA 4488, IFR 114, Université Lille 1, Sciences et Technologies, Villeneuve d'Ascq, France.
authors.forename: Erwan
authors.initials: E
authors.lastname: Dupont
mesh_terms: D000818:Animals; D002540:Cerebral Cortex / Q000502:physiology*; D015870:Gene Expression; D007103:Immobilization; D007334:Insulin-Like Growth Factor I / Q000378:metabolism*; D008297:Male; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D011597:Psychomotor Performance; D051381:Rats; D017526:Receptor, IGF Type 1 / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D007334:Insulin-Like Growth Factor I; D019869:Phosphatidylinositol 3-Kinases; D017526:Receptor, IGF Type 1; D051057:Proto-Oncogene Proteins c-akt