Maintenance of eupnea of in situ and in vivo rats following riluzole: A blocker of persistent sodium channels
2007 | journal article. A publication with affiliation to the University of Göttingen.
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Maintenance of eupnea of in situ and in vivo rats following riluzole: A blocker of persistent sodium channels
St.-John, W. A.; Waki, H.; Dutschmann, M. & Paton, J. F. R. (2007)
Respiratory Physiology & Neurobiology, 155(1) pp. 97-100. DOI: https://doi.org/10.1016/j.resp.2006.04.018
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- Authors
- St.-John, Walter A.; Waki, Hidefumi; Dutschmann, Mathias; Paton, Julian F. R.
- Abstract
- We have proposed a "switching" concept for the neurogenesis of breathing in which rhythm generation by a pontomedullary neuronal circuit for eupnea may be switched to a medullary pacemaker system for gasping. This switch involves activation of conductances through persistent sodium channels. Based upon this proposal, eupnea should continue following a blockade of persistent sodium channels. In situ preparations of the decerebrate, juvenile rat were studied in normocapnia, hypocapnia and hypercapnia. Regardless of the level of CO(2) drive, riluzole (1-10 mu M), a blocker of persistent sodium channels, caused increases in the frequency and reductions in peak integrated phrenic height. Even 20 mu M of riluzole, a concentration four-fold higher than that which eliminates gasping, did not cause a cessation of phrenic discharge. In conscious, rats breathing continued unabated following intravenous administrations of 3-9 mg kg(-1) of riluzole. These administrations did cause sedation. We conclude that conductance through persistent sodium channels plays little role in the neurogenesis of eupnea. (c) 2006 Elsevier B.V. All rights reserved.
- Issue Date
- 2007
- Status
- published
- Publisher
- Elsevier Science Bv
- Journal
- Respiratory Physiology & Neurobiology
- ISSN
- 1569-9048
- Sponsor
- NHLBI NIH HHS [HL26091]; Wellcome Trust