Literature DB >> 27717815

Reorganization of motor cortex and impairment of motor performance induced by hindlimb unloading are partially reversed by cortical IGF-1 administration.

Julien Mysoet1, Marie-Hélène Canu2, Christophe Gillet3, Julie Fourneau4, Cyril Garnier5, Bruno Bastide6, Erwan Dupont7.   

Abstract

Immobilization, bed rest, or sedentary lifestyle, are known to induce a profound impairment in sensorimotor performance. These alterations are due to a combination of peripheral and central factors. Previous data conducted on a rat model of disuse (hindlimb unloading, HU) have shown a profound reorganization of motor cortex and an impairment of motor performance. Recently, our interest was turned towards the role of insulin-like growth factor 1 (IGF-1) in cerebral plasticity since this growth factor is considered as the mediator of beneficial effects of exercise on the central nervous system, and its cortical level is decreased after a 14-day period of HU. In the present study, we attempted to determine whether a chronic subdural administration of IGF-1 in HU rats could prevent deleterious effects of HU on the motor cortex and on motor activity. We demonstrated that HU induces a shrinkage of hindlimb cortical representation and an increase in current threshold to elicit a movement. Administration of IGF-1 in HU rats partially reversed these changes. The functional evaluation revealed that IGF-1 prevents the decrease in spontaneous activity found in HU rats and the changes in hip kinematics during overground locomotion, but had no effect of challenged locomotion (ladder rung walking test). Taken together, these data clearly indicate the implication of IGF-1 in cortical plastic mechanisms and in behavioral alteration induced by a decreased in sensorimotor activity.
Copyright © 2016 Elsevier B.V. All rights reserved.

Entities:  

Keywords:  Actimetry; Cortical plasticity; Disuse; Kinematics; Locomotion; Motor performance

Mesh:

Substances:

Year:  2016        PMID: 27717815     DOI: 10.1016/j.bbr.2016.10.005

Source DB:  PubMed          Journal:  Behav Brain Res        ISSN: 0166-4328            Impact factor:   3.332


  3 in total

1.  Tau deletion promotes brain insulin resistance.

Authors:  Elodie Marciniak; Antoine Leboucher; Emilie Caron; Tariq Ahmed; Anne Tailleux; Julie Dumont; Tarik Issad; Ellen Gerhardt; Patrick Pagesy; Margaux Vileno; Clément Bournonville; Malika Hamdane; Kadiombo Bantubungi; Steve Lancel; Dominique Demeyer; Sabiha Eddarkaoui; Emmanuelle Vallez; Didier Vieau; Sandrine Humez; Emilie Faivre; Benjamin Grenier-Boley; Tiago F Outeiro; Bart Staels; Philippe Amouyel; Detlef Balschun; Luc Buee; David Blum
Journal:  J Exp Med       Date:  2017-06-26       Impact factor: 14.307

2.  Knock-in of Mutated hTAU Causes Insulin Resistance, Inflammation and Proteostasis Disturbance in a Mouse Model of Frontotemporal Dementia.

Authors:  Claire Hull; Ruta Dekeryte; David J Koss; Barry Crouch; Heather Buchanan; Mirela Delibegovic; Bettina Platt
Journal:  Mol Neurobiol       Date:  2019-08-08       Impact factor: 5.590

3.  Overexpression of catalase in mitochondria mitigates changes in hippocampal cytokine expression following simulated microgravity and isolation.

Authors:  Linda Rubinstein; Ann-Sofie Schreurs; Samantha M Torres; Sonette Steczina; Moniece G Lowe; Frederico Kiffer; Antiño R Allen; April E Ronca; Marianne B Sowa; Ruth K Globus; Candice G T Tahimic
Journal:  NPJ Microgravity       Date:  2021-07-06       Impact factor: 4.415

  3 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.