title: Effects of galvanic vestibular stimulation on postural limb reflexes and neurons of spinal postural network.
abstract: Quadrupeds maintain the dorsal side up body orientation due to the activity of the postural control system driven by limb mechanoreceptors. Binaural galvanic vestibular stimulation (GVS) causes a lateral body sway toward the anode. Previously, we have shown that this new position is actively stabilized, suggesting that GVS changes a set point in the reflex mechanisms controlling body posture. The aim of the present study was to reveal the underlying neuronal mechanisms. Experiments were performed on decerebrate rabbits. The vertebral column was rigidly fixed, whereas hindlimbs were positioned on a platform. Periodic lateral tilts of the platform caused postural limb reflexes (PLRs): activation of extensors in the loaded and flexing limb and a decrease in extensor activity in the opposite (unloaded and extending) limb. Putative spinal interneurons were recorded in segments L4-L5 during PLRs, with and without GVS. We have found that GVS enhanced PLRs on the cathode side and reduced them on the anode side. This asymmetry in PLRs can account for changes in the stabilized body orientation observed in normal rabbits subjected to continuous GVS. Responses to platform tilts (frequency modulation) were observed in 106 spinal neurons, suggesting that they can contribute to PLR generation. Two neuron groups were active in opposite phases of the tilt cycle of the ipsi-limb: F-neurons in the flexion phase, and E-neurons in the extension phase. Neurons were driven mainly by afferent input from the ipsi-limb. If one supposes that F- and E-neurons contribute, respectively, to excitation and inhibition of extensor motoneurons, one can expect that the pattern of response to GVS in F-neurons will be similar to that in extensor muscles, whereas E-neurons will have an opposite pattern. We have found that ~40% of all modulated neurons meet this condition, suggesting that they contribute to the generation of PLRs and to the GVS-caused changes in PLRs.
authors.affiliation: Department of Neuroscience, Karolinska Institute, Stockholm, Sweden.
authors.forename: L-J
authors.initials: LJ
authors.lastname: Hsu
authors.forename: P V
authors.initials: PV
authors.lastname: Zelenin
authors.forename: G N
authors.initials: GN
authors.lastname: Orlovsky
authors.forename: T G
authors.initials: TG
authors.lastname: Deliagina
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D003655:Decerebrate State; D004558:Electric Stimulation / Q000379:methods; D005121:Extremities / Q000502:physiology*; D007839:Functional Laterality / Q000502:physiology; D009433:Neural Inhibition / Q000502:physiology; D009474:Neurons / Q000145:classification / Q000502:physiology*; D011187:Posture / Q000502:physiology*; D011817:Rabbits; D012018:Reflex / Q000502:physiology*; D013116:Spinal Cord / Q000166:cytology* / Q000502:physiology; D014725:Vestibular Nerve / Q000502:physiology*