title: [Toward a metabolic approach of the central pattern generator concept in a spinal rat model].
abstract: It has been shown that the onset of a central nervous system lesion in the rat results in morphological modifications of the peripheral nerves and the underlying neuromuscular junctions, without suggesting a functional correlation between recuperation of motor functions and sublesional metabolic activity. Using double lesion localization (T2 and T6) in a spinal rat model has nevertheless pointed out the functional importance of the T2-T6 metameric interval in the reinnervation phenomena observed, raising the problem of spinal generation in locomotor movements. Motivated by electrophysiological data that have given support to the concept of an anatomic substrate for these intramedullary rhythm generators, we attempted to establish a relation between the functional recuperation possible after a central nervous system lesion and modifications within the metabolism of the underlying neuromuscular system. We notably focused on Na/K-ATPase, whose crucial role in neuromuscular transmission has been evidenced. This paper proposes to demonstrate the involvement in the mechanisms of metabolic regulation after trans-synaptic denervation, i.e., a central nervous system lesion. Our study includes the Na/K-ATPase activity analysis on the sublesional peripheral nerve and the combined analysis of the expression of different RNA messengers within the corresponding muscle groups. We have also investigated the spatiotemporal organization of the compensating processes of the nerves underlying the lesion using magnetic resonance spectroscopy.
authors.affiliation: Service de neurochirurgie, CHU La Milétrie, 2, rue de la Milétrie, BP 577, 86021 Poitiers cedex, France. p.rigoard@chu-poitiers.fr
authors.forename: P
authors.initials: P
authors.lastname: Rigoard
authors.forename: K
authors.initials: K
authors.lastname: Buffenoir
authors.forename: M
authors.initials: M
authors.lastname: Fares
authors.forename: M
authors.initials: M
authors.lastname: Chaillou
authors.forename: L
authors.initials: L
authors.lastname: Da Costa
authors.forename: N
authors.initials: N
authors.lastname: Boildieu
authors.forename: F
authors.initials: F
authors.lastname: Seguin
authors.forename: C
authors.initials: C
authors.lastname: Huze
authors.forename: L
authors.initials: L
authors.lastname: Schaeffer
authors.forename: F
authors.initials: F
authors.lastname: Lapierre
authors.forename: J-M
authors.initials: JM
authors.lastname: Maixent
mesh_terms: D000818:Animals; D003655:Decerebrate State / Q000378:metabolism* / Q000503:physiopathology*; D004594:Electrophysiology; D005260:Female; D007323:Instinct; D008279:Magnetic Resonance Imaging; D009068:Movement / Q000502:physiology; D009121:Muscle Denervation; D009419:Nerve Tissue Proteins / Q000378:metabolism; D010525:Peripheral Nerves / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism / Q000502:physiology; D009435:Synaptic Transmission / Q000502:physiology; D013979:Tibial Nerve / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure
chemical_list: D009419:Nerve Tissue Proteins; D000254:Sodium-Potassium-Exchanging ATPase