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Am J Physiol Regul Integr Comp Physiol (July 8, 2002). doi:10.1152/ajpregu.00004.2002
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Articles in PresS, published online ahead of print July 4, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00004.2002
Submitted on January 7, 2002
Accepted on June 10, 2002

Potential switch from eupnea to fictive gasping following blockade of glycine transmission and potassium channels

Walter M St.-John1, Ilya A Rybak2*, and Julian F. R Paton3

1 Department of Physiology, Dartmouth Medical School, Lebanon, NH, USA
2 Science and Health Systems, School of Biomedical Engineering, Drexel University, Philadelphia, PA, USA
3 Department of Physiology, School of Medical Sciences, University of Bristol, Bristol, UK

* To whom correspondence should be addressed. E-mail: rybak{at}cbis.ece.drexel.edu.

This study evaluated possible neuronal mechanisms responsible for the transition from normal breathing (eupnea) to gasping. We hypothesized that a blockade of both inhibitory glycinergic synaptic transmission and potassium channels, combined with an increase in extracellular concentration of potassium, would induce a switch from an eupneic respiratory pattern to gasping. Efferent activities of the phrenic, vagal and hypoglossal nerves were recorded during eupnea and ischemia-induced gasping in a perfused in situ preparation of the juvenile rat (4-6 weeks of age). To block potassium channels, 4-aminopyridine (4-AP, 1-10 µM) was administered. Strychnine (0.2-0.6 µM) was used to block glycinergic neurotransmission. Following administrations of 4-AP, excess extracellular potassium (10.25-17.25 mM) and strychnine, the incrementing pattern of eupneic phrenic activity was altered to a decrementing discharge. Hypoglossal and vagal activities became concentrated to the period of the phrenic burst with expiratory activity being reduced or eliminated. These changes in neural activities were similar to those in ischemia-induced gasping. Results are consistent with the concept that the elicitation of gasping represents a switch from a network-based rhythmogenesis for eupnea to a pacemaker-driven mechanism.




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