Spinal interneurons that receive input from muscle afferents are differentially modulated by dorsolateral descending systems

Citation
Df. Chen et al., Spinal interneurons that receive input from muscle afferents are differentially modulated by dorsolateral descending systems, J NEUROPHYS, 85(2), 2001, pp. 1005-1008
Citations number
16
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROPHYSIOLOGY
ISSN journal
00223077 → ACNP
Volume
85
Issue
2
Year of publication
2001
Pages
1005 - 1008
Database
ISI
SICI code
0022-3077(200102)85:2<1005:SITRIF>2.0.ZU;2-J
Abstract
The possibility that descending systems have differential actions on the sp inal interneurons that receive input from muscle afferents was investigated . Prolonged, physiological inputs were generated by stretch of the triceps surae muscles. The resulting firing patterns of 25 lumbosacral interneurons were recorded before and during a reversible cold block of the dorsolatera l white matter at the thoracic level in nonparalyzed, decerebrate preparati ons. The strength of group I muscle afferent input was assessed from the re sponse to sinusoidal tendon vibration, which activated muscle spindle Ia af ferents directly and tendon organ Ib afferents via the resulting reflex for ce. The stretch-evoked responses of interneurons with strong responses to v ibration were markedly suppressed by dorsal cold block, whereas the stretch -evoked responses of interneurons with weak vibration input were enhanced. The cells most strongly activated by vibration received their primary input from Ia afferents and all of these cells were inhibited by the cold block. These results suggest that a disruption of the descending system, such as occurs in spinal cord injury, will lead to a suppression of the interneuron al pathways with group Ia input while enhancing excitability within interne uronal pathways transmitting actions from higher threshold afferents. One p ossible consequence of this suppression would be a decreased activity among the Ia inhibitory interneurons that mediate reciprocal inhibition, resulti ng in abnormal reciprocal relations between antagonists and promoting anoma lous muscle cocontraction.