HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 289/6/H2575    most recent 00585.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by Degtyarenko, A. M. Articles by Kaufman, M. P. Search for Related Content PubMed PubMed Citation Articles by Degtyarenko, A. M. Articles by Kaufman, M. P.

MLR-induced inhibition of barosensory cells in the NTS

Division of Cardiovascular Medicine, Departments of Internal Medicine and Human Physiology, University of California, Davis, California

Submitted 3 June 2005 ; accepted in final form 26 July 2005

A central motor command arising from the mesencephalic locomotor region (MLR) is widely believed to be one of the neural mechanisms that reset the baroreceptor reflex upward during exercise. The nucleus tractus solitarius (NTS), a dorsal medullary site that receives input from baroreceptors, may be the site where central command inhibits baroreceptor input during exercise. We, therefore, examined the effect of electrical stimulation of the MLR on the impulse activity of cells in the NTS in decerebrate paralyzed cats. Of 129 NTS cells tested for baroreceptor input by injection of phenylephrine (7–25 µg/kg iv) or inflation of a balloon in the carotid sinus, 58 were stimulated and 19 were inhibited. MLR stimulation (80–150 µA) inhibited the discharge of 48 of the 58 cells stimulated by baroreceptor input. MLR stimulation had no effect on the discharge of the remaining 10 cells, each of which displayed no spontaneous activity. In contrast to the 77 NTS cells responsive to baroreceptor input, there was no change in activity of 52 cells when arterial pressure was increased by phenylephrine injection or balloon inflation. MLR stimulation activated each of the 52 NTS cells. For 23 of the cells, the onset latency to MLR stimulation was clearly discernable, averaging 6.4 ± 0.4 ms. Our findings provide electrophysiological evidence for the hypothesis that the MLR inhibits the baroreceptor reflex by activating NTS interneurons unresponsive to baroreceptor input. In turn, these interneurons may release an inhibitory neurotransmitter onto NTS cells receiving baroreceptor input.

exercise; central command; baroreceptor reflex; cats; autonomic nervous system

This article has been cited by other articles:

				L. C. Michelini and J. E. Stern Exercise-induced neuronal plasticity in central autonomic networks: role in cardiovascular control Exp Physiol, September 1, 2009; 94(9): 947 - 960. [Abstract] [Full Text] [PDF]

				C.-Y. Chen, A. G. Bechtold, J. Tabor, and A. C. Bonham Exercise Reduces GABA Synaptic Input onto Nucleus Tractus Solitarii Baroreceptor Second-Order Neurons via NK1 Receptor Internalization in Spontaneously Hypertensive Rats J. Neurosci., March 4, 2009; 29(9): 2754 - 2761. [Abstract] [Full Text] [PDF]

				W.-Z. Wang, L. Gao, Y.-X. Pan, I. H. Zucker, and W. Wang AT1 receptors in the nucleus tractus solitarii mediate the interaction between the baroreflex and the cardiac sympathetic afferent reflex in anesthetized rats Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1137 - R1145. [Abstract] [Full Text] [PDF]

				T. G. Waldrop, G. A. Iwamoto, and P. Haouzi Point:Counterpoint: Supraspinal locomotor centers do/do not contribute significantly to the hyperpnea of dynamic exercise J Appl Physiol, March 1, 2006; 100(3): 1077 - 1083. [Full Text] [PDF]