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Am J Physiol Regul Integr Comp Physiol 279: R639-R649, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 2, R639-R649, August 2000

Relative magnitude of tonic and phasic synaptic excitation of medullary inspiratory neurons in dogs

M. Krolo1,2, E. A. Stuth1,2, M. Tonkovic-Capin1,2, F. A. Hopp1,2, D. R. McCrimmon3, and E. J. Zuperku1,2

1 Zablocki Veterans Affairs Medical Center, Milwaukee 53295; 2 Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226; and 3 Department of Physiology and Institute for Neuroscience, Northwestern University Medical School, Chicago, Illinois 60611

The relative contribution of phasic and tonic excitatory synaptic drives to the augmenting discharge patterns of inspiratory (I) neurons within the ventral respiratory group (VRG) was studied in anesthetized, ventilated, paralyzed, and vagotomized dogs. Multibarrel micropipettes were used to record simultaneously single-unit neuronal activity and pressure microejected antagonists of GABAergic, glycinergic, N-methyl-D-aspartate (NMDA) and non-NMDA glutamatergic, and cholinergic receptors. The discharge patterns were quantified via cycle-trigger histograms. The findings suggest that two-thirds of the excitatory drive to caudal VRG I neurons is tonic and mediated by NMDA receptors and the other third is ramp-like phasic and mediated by non-NMDA receptors. Cholinergic receptors do not appear to be involved. The silent expiratory phase is produced by phasic inhibition of the tonic activity, and approx 80% of this inhibition is mediated by gamma -aminobutyric acid receptors (GABAA) and approx 20% by glycine receptors. Phasic I inhibition by the I decrementing neurons does not appear to contribute to the predominantly step-ramp patterns of these I neurons. However, this decrementing inhibition may be very prominent in controlling the rate of augmentation in late-onset I neurons and those with ramp patterns lacking the step component.

control of breathing; central pattern generation; neurotransmitters; gamma -aminobutyric acid receptors; glutamatergic receptors


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