title: Training locomotor networks.
abstract: For a complete adult spinal rat to regain some weight-bearing stepping capability, it appears that a sequence of specific proprioceptive inputs that are similar, but not identical, from step to step must be generated over repetitive step cycles. Furthermore, these cycles must include the activation of specific neural circuits that are intrinsic to the lumbosacral spinal cord segments. For these sensorimotor pathways to be effective in generating stepping, the spinal circuitry must be modulated to an appropriate excitability level. This level of modulation is sustained from supraspinal input in intact, but not spinal, rats. In a series of experiments with complete spinal rats, we have shown that an appropriate level of excitability of the spinal circuitry can be achieved using widely different means. For example, this modulation level can be acquired pharmacologically, via epidural electrical stimulation over specific lumbosacral spinal cord segments, and/or by use-dependent mechanisms such as step or stand training. Evidence as to how each of these treatments can "tune" the spinal circuitry to a "physiological state" that enables it to respond appropriately to proprioceptive input will be presented. We have found that each of these interventions can enable the proprioceptive input to actually control extensive details that define the dynamics of stepping over a range of speeds, loads, and directions. A series of experiments will be described that illustrate sensory control of stepping and standing after a spinal cord injury and the necessity for the "physiological state" of the spinal circuitry to be modulated within a critical window of excitability for this control to be manifested. The present findings have important consequences not only for our understanding of how the motor pattern for stepping is formed, but also for the design of rehabilitation intervention to restore lumbosacral circuit function in humans following a spinal cord injury.
authors.affiliation: Department of Physiological Science, University of California, Los Angeles, Los Angeles, CA 90095, USA. vre@ucla.edu
authors.forename: V Reggie
authors.initials: VR
authors.lastname: Edgerton
authors.forename: Grégoire
authors.initials: G
authors.lastname: Courtine
authors.forename: Yury P
authors.initials: YP
authors.lastname: Gerasimenko
authors.forename: Igor
authors.initials: I
authors.lastname: Lavrov
authors.forename: Ronaldo M
authors.initials: RM
authors.lastname: Ichiyama
authors.forename: Andy J
authors.initials: AJ
authors.lastname: Fong
authors.forename: Lance L
authors.initials: LL
authors.lastname: Cai
authors.forename: Chad K
authors.initials: CK
authors.lastname: Otoshi
authors.forename: Niranjala J K
authors.initials: NJ
authors.lastname: Tillakaratne
authors.forename: Joel W
authors.initials: JW
authors.lastname: Burdick
authors.forename: Roland R
authors.initials: RR
authors.lastname: Roy
mesh_terms: D000818:Animals; D006801:Humans; D007858:Learning / Q000502:physiology; D008124:Locomotion / Q000187:drug effects / Q000502:physiology*; D009415:Nerve Net / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology; D013119:Spinal Cord Injuries / Q000188:drug therapy / Q000503:physiopathology