title: Restricted neural plasticity in vestibulospinal pathways after unilateral labyrinthectomy as the origin for scoliotic deformations.
abstract: Adolescent idiopathic scoliosis in humans is often associated with vestibulomotor deficits. Compatible with a vestibular origin, scoliotic deformations were provoked in adult Xenopus frogs by unilateral labyrinthectomy (UL) at larval stages. The aquatic ecophysiology and absence of body-weight-supporting limb proprioceptive signals in amphibian tadpoles as a potential sensory substitute after UL might be the cause for a persistent asymmetric descending vestibulospinal activity. Therefore, peripheral vestibular lesions in larval Xenopus were used to reveal the morphophysiological alterations at the cellular and network levels. As a result, spinal motor nerves that were modulated by the previously intact side before UL remained permanently silent during natural vestibular stimulation after the lesion. In addition, retrograde tracing of descending pathways revealed a loss of vestibular neurons on the ipsilesional side with crossed vestibulospinal projections. This loss facilitated a general mass imbalance in descending premotor activity and a permanent asymmetric motor drive to the axial musculature. Therefore, we propose that the persistent asymmetric contraction of trunk muscles exerts a constant, uncompensated differential mechanical pull on bilateral skeletal elements that enforces a distortion of the soft cartilaginous skeletal elements and bone shapes. This ultimately provokes severe scoliotic deformations during ontogenetic development similar to the human syndrome.
authors.affiliation: Centre d'Etude de la SensoriMotricité, Centre National de la Recherche Scientifique Unité Mixte de Recherche 8194, Université Paris Descartes, 75006 Paris, France.
authors.forename: François M
authors.initials: FM
authors.lastname: Lambert
authors.forename: David
authors.initials: D
authors.lastname: Malinvaud
authors.forename: Maxime
authors.initials: M
authors.lastname: Gratacap
authors.forename: Hans
authors.initials: H
authors.lastname: Straka
authors.forename: Pierre-Paul
authors.initials: PP
authors.lastname: Vidal
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D005452:Fluoresceins / Q000378:metabolism; D007839:Functional Laterality / Q000502:physiology*; D066298:In Vitro Techniques; D007814:Larva; D008297:Male; D009135:Muscular Diseases / Q000209:etiology; D009434:Neural Pathways; D019636:Neurodegenerative Diseases / Q000209:etiology*; D009473:Neuronal Plasticity / Q000502:physiology*; D012600:Scoliosis / Q000209:etiology*; D012678:Sensation Disorders / Q000209:etiology; D013116:Spinal Cord / Q000502:physiology*; D018709:Statistics, Nonparametric; D013997:Time Factors; D014722:Vestibule, Labyrinth / Q000293:injuries* / Q000502:physiology*; D000160:Vestibulocochlear Nerve Diseases / Q000150:complications*; D014981:Xenopus
chemical_list: D005452:Fluoresceins; C007740:fluorexon