Spasticity of the midline musculature can significantly hinder performing transfers and lead to development of pressure sores. Currently, significant gaps exist in our knowledge of the pathophysiology involved in spasticity development following SCI, especially regarding the axial musculature. The goals of this study were: (1) to determine the effects of S2 transection on the number and distribution of glutamatergic, GABAergic and cholinergic inputs on more caudal motoneurons, (2) to correlate these changes with the development of spasticity within the tail musculature, which are the caudal counterparts to the axial musculature. Animals with S2 spinal transection were tested behaviorally for the progression of spasticity within the tail musculature. At 1, 2, 4, or 12 weeks post-injury, the animals were sacrificed and temporal changes in glutamatergic, GABAergic, and cholinergic inputs to sacrocaudal motoneurons were assessed using antibodies for the specific vesicular transporter of each neurotransmitter and confocal microscopy. At 1 week post-injury, when the tail musculature demonstrated decreased responsiveness, an overall increase in the ratio of excitatory to inhibitory input to sacrocaudal motoneurons was observed. From 2 to 12 weeks post-injury, when the tail musculature demonstrated increased reflex behavior, an overall decrease in the ratio of excitatory to inhibitory inputs was observed. Additionally, from 2 to 12 weeks following spinal transection, a progressive loss of cholinergic labeling of sacrocaudal motoneurons was observed. The increase in the overall level of excitation with a concomitant loss of cholinergic influence following spinal transection could, in part, explain the development of spasticity within the tail musculature.
|Number of pages||13|
|State||Published - Feb 2006|
Bibliographical noteFunding Information:
The author would like to thank Ms. Alyssa Moore for her assistance in the analysis of the confocal images. This work was supported by grants from The American Paraplegia Society (#892), the University of Kentucky Executive Vice President for Research: Research Support grant, and the Kentucky Spinal Cord and Head Injury Research Trust.
- Neurotransmitter transporters
ASJC Scopus subject areas
- Developmental Neuroscience