Effect of acute lateral hemisection of the spinal cord on spinal neurons of postural networks

- Acute lateral hemisection (LHS) of the spinal cord causes right-left asymmetry in postural limb reflexes.
- We examine the effects of acute LHS on two populations of spinal interneurons (F and E) mediating postural limb reflexes.
- LHS causes a reduction in the proportion of F-neurons on the lesioned side.
- LHS causes a reduction in activity of E- and F-neurons located in specific areas of the gray matter.
- These activity changes are due to specific changes in the efficacy of posture-related sensory inputs to F- and E-neurons.

In quadrupeds, acute lateral hemisection of the spinal cord (LHS) severely impairs postural functions, which recover over time. Postural limb reflexes (PLRs) represent a substantial component of postural corrections in intact animals. The aim of the present study was to characterize the effects of acute LHS on two populations of spinal neurons (F and E) mediating PLRs. For this purpose, in decerebrate rabbits, responses of individual neurons from L5 to stimulation causing PLRs were recorded before and during reversible LHS (caused by temporal cold block of signal transmission in lateral spinal pathways at L1), as well as after acute surgical LHS at L1. Results obtained after Sur-LHS were compared to control data obtained in our previous study.We found that acute LHS caused disappearance of PLRs on the affected side. It also changed a proportion of different types of neurons on that side. A significant decrease and increase in the proportion of F- and non-modulated neurons, respectively, was found. LHS caused a significant decrease in most parameters of activity in F-neurons located in the ventral horn on the lesioned side and in E-neurons of the dorsal horn on both sides. These changes were caused by a significant decrease in the efficacy of posture-related sensory input from the ipsilateral limb to F-neurons, and from the contralateral limb to both F- and E-neurons. These distortions in operation of postural networks underlie the impairment of postural control after acute LHS, and represent a starting point for the subsequent recovery of postural functions.