Details

Autor(en) / Beteiligte

• Chen, Daofen
• Theiss, Renee D
• Ebersole, Koji
• Miller, John F
• Rymer, W. Zev
• Heckman, C. J

Titel

Spinal Interneurons That Receive Input From Muscle Afferents Are Differentially Modulated by Dorsolateral Descending Systems

Ist Teil von

• Journal of neurophysiology, 2001-02, Vol.85 (2), p.1005-1008

Ort / Verlag

United States: Am Phys Soc

Erscheinungsjahr

2001

Quelle

Free E-Journal (出版社公開部分のみ）

Beschreibungen/Notizen

•   1 Departments of Physiology and Physical Medicine and Rehabilitation, Northwestern University Medical School; and   2 Veterans Administration, Lakeside Hospital, Chicago, Illinois 60611 Chen, Daofen, Renee D. Theiss, Koji Ebersole, John F. Miller, W. Zev Rymer, and C. J. Heckman. Spinal Interneurons That Receive Input From Muscle Afferents Are Differentially Modulated by Dorsolateral Descending Systems. J. Neurophysiol. 85: 1005-1008, 2001. The possibility that descending systems have differential actions on the spinal 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 dorsolateral white matter at the thoracic level in nonparalyzed, decerebrate preparations. The strength of group I muscle afferent input was assessed from the response to sinusoidal tendon vibration, which activated muscle spindle Ia afferents directly and tendon organ Ib afferents via the resulting reflex force. The stretch-evoked responses of interneurons with strong responses to vibration 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 interneuronal pathways with group Ia input while enhancing excitability within interneuronal pathways transmitting actions from higher threshold afferents. One possible consequence of this suppression would be a decreased activity among the Ia inhibitory interneurons that mediate reciprocal inhibition, resulting in abnormal reciprocal relations between antagonists and promoting anomalous muscle cocontraction.