Balance Control Mediated by Vestibular Circuits Directing Limb Extension or Antagonist Muscle Co-activation

Abstract

Maintaining balance after an external perturbation requires modification of ongoing motor plans and the selection of contextually appropriate muscle activation patterns that respect body and limb position. We have used the vestibular system to generate sensory-evoked transitions in motor programming. In the face of a rapid balance perturbation, the lateral vestibular nucleus (LVN) generates exclusive extensor muscle activation and selective early extension of the hindlimb, followed by the co-activation of extensor and flexor muscle groups. The temporal separation in EMG response to balance perturbation reflects two distinct cell types within the LVN that generate different phases of this motor program. Initially, an LVN population directs an extension movement that reflects connections with extensor, but not flexor, motor neurons. A distinct LVN population initiates muscle co-activation via the pontine reticular nucleus. Thus, distinct circuits within the LVN generate different elements of a motor program involved in the maintenance of balance.

Current Principles of Motor Control, with Special Reference to Vertebrate Locomotion

“…Also in mammals, the vestibular control is important in that it detects movements of the head, which can be used for rapid compensations, and an asymmetric activation of the vestibular apparatus leads to changes in posture during standing and also during locomotion (114,115,118,121,135,353). These effects are mediated primarily by the vestibulospinal projections from Deiters nucleus, which convey monosynaptic excitation to extensor motoneurons (216,350).…”

Spinal dI2 interneurons regulate the stability of bipedal stepping

“…Mammalian VSCT neurons receive descending input from reticulospinal, rubrospinal and vestibulospinal pathways (Bras et al, 1988, Jankowska andHammar, 2013). Neurons from the lateral vestibular nucleus, have been reported to innervate extensor motoneurons at the lumbar level, as well as interneurons residing at the medial lamina VII (Murray et al, 2018), exactly at the location where dI2…”

Motor cortical inactivation reduces the gain of kinematic primitives in mice performing a hold-still center-out reach task

“…The generation, direction and timing of submillimeter-scale primitives produced during the hold were surprisingly intact during cortical inactivations, suggesting that subcortical pathways are sufficient to produce corrective movements required for postural control during holding-still (Azim et al, 2014;Murray et al, 2018;Walter et al, 2006). However, the change in the offset, slope, and inflection point of the SDF observed during motor cortical inactivation suggests that, although the cortex is not required for the performance of the hold, it could modulate corrective processes underlying postural stability.…”