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J Neurophysiol 87: 1664-1668, 2002;
0022-3077/02 $5.00
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The Journal of Neurophysiology Vol. 87 No. 3 March 2002, pp. 1664-1668
Copyright ©2002 by the American Physiological Society

RAPID COMMUNICATION

Modulation of Gasp Frequency by Activation of Pre-Bötzinger Complex In Vivo

Irene C. Solomon

Department of Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, New York 11794-8661

Solomon, Irene C. Modulation of Gasp Frequency by Activation of Pre-Bötzinger Complex In Vivo. J. Neurophysiol. 87: 1664-1668, 2002. Under hyperoxic conditions, both chemical stimulation of neurons and focal hypoxia in the pre-Bötzinger complex (pre-BötC) in vivo modify the eupneic pattern of inspiratory motor output by eliciting changes in the patterning and timing of phrenic bursts, which includes both phasic and tonic excitation. The influence of this region on the gasping pattern of phrenic motor output produced during severe brain hypoxia is unknown. We therefore examined the effects of chemical stimulation of neurons (DL-homocysteic acid; DLH; 10 mM; <= 20 nl) and focal hypoxia (sodium cyanide; NaCN; 1 mM; <= 20 nl) in the pre-BötC on hypoxia-induced gasping in chloralose-anesthetized, vagotomized, mechanically ventilated cats. Unilateral microinjection of DLH into the pre-BötC during hypoxia-induced gasping increased phrenic burst frequency by ~630% (P < 0.01) over baseline frequency due predominantly to a reduction in TE (from 28.9 ± 6.2 to 5.2 ± 1.8 s; mean ± SE; P < 0.01). No significant changes in TI or rate of rise between hypoxia-induced gasps and the DLH-induced bursts were observed; the effects on peak amplitude of integrated phrenic nerve discharge were variable. Similar responses were evoked by unilateral microinjection of NaCN into the pre-BötC. These findings demonstrate that both activation of pre-BötC neurons and focal hypoxia in the pre-BötC not only influence the eupneic pattern of phrenic motor output but also modify the expression of hypoxia-induced gasping in vivo. These findings also provide additional support to the concept of intrinsic hypoxic chemosensitivity of the pre-BötC.




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