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Am J Physiol Regul Integr Comp Physiol (June 20, 2002). doi:10.1152/ajpregu.00054.2002
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Articles in PresS, published online ahead of print June 20, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00054.2002
Submitted on January 29, 2002
Accepted on June 18, 2002

Chemical activation of C1-C2 spinal neurons modulates activity of thoracic respiratory interneurons in rats

C. Qin1*, J. P Farber1, M. J Chandler1, and P. D Foreman1

1 Department of Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA

* To whom correspondence should be addressed. E-mail: chao-qin{at}ouhsc.edu.

Discharge patterns of thoracic dorsal horn neurons are influenced by chemical activation of cell bodies in C1-C2. The present aim was to examine whether such activation would specifically affect thoracic respiratory interneurons (TRINs) of the deep dorsal horn and intermediate zone in pentobarbital anesthetized, paralyzed, artificially ventilated rats. We also characterized discharge patterns and pathways of TRIN activation in rats. A total of 77 cells were classified as TRINs by location, continued burst activity related to phrenic discharge when the respirator was stopped, and lack of antidromic response from selected pathways. A variety of respiration-phased discharge patterns were documented whose pathways were interrupted by ipsilateral C1 transection. Glutamate pledgets (1M, 1 min) on the dorsal surface of the spinal cord inhibited 22/49, excited 15/49, or excited/inhibited 3/49 tested cells. Incidence of responses did not depend upon whether the phase of TRIN discharge was inspiratory, expiratory, or biphasic. Phrenic nerve activity was unaffected by chemical activation of C1 -C2 in this preparation. Besides supraspinal input, TRIN activity may be influenced by upper cervical modulatory pathways.




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