JN Journal of Neurophysiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Neurophysiol 61: 918-926, 1989;
0022-3077/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Bolser, D. C.
Right arrow Articles by Remmers, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Bolser, D. C.
Right arrow Articles by Remmers, J. E.

Journal of Neurophysiology, Vol 61, Issue 5 918-926, Copyright © 1989 by APS

ARTICLES

Synaptic effects of intercostal tendon organs on membrane potentials of medullary respiratory neurons

D. C. Bolser and J. E. Remmers
Department of Medicine, University of Calgary Health Sciences Center, Alberta, Canada.

1. Stimulation of intercostal muscle tendon organs or their afferent fibers reduces medullary inspiratory neuron activity, decreases motor output to inspiratory muscles, and increases the activity of expiratory laryngeal motoneurons. The present study examines the synaptic mechanisms underlying these changes to obtain information about medullary neurons that participate in the afferent limb of this reflex pathway. 2. Membrane potentials of medullary respiratory neurons were recorded in decerebrate paralyzed cats. Postsynaptic potentials (PSPs) elicited in these neurons by intercostal nerve stimulation (INS) were compared before and after intracellular iontophoresis of chloride ions. After chloride injection, the normal hyperpolarization caused by inhibitory (I) PSPs is "reversed" to depolarization. 3. In inspiratory neurons, reversal of IPSPs by chloride injection also reversed hyperpolarization produced by INS when applied during any portion of the respiratory cycle. This observation suggests that increased chloride conductance of the postsynaptic membrane mediated the inhibition. Further, it is very likely that the last-order interneuron in the afferent pathway must be excited by INS and alter inspiratory neuron activity via an inhibitory synapse. The linear relationship between the amplitude of the INS induced PSP and membrane potential of inspiratory neurons provided evidence that neurons in the afferent pathway are not respiratory modulated. 4. The membranes of expiratory vagal motoneurons and post-inspiratory neurons were depolarized by INS during all portions of the respiratory cycle before IPSP reversal. Reversal of IPSPs affected neither this depolarization of expiratory vagal motoneurons during stage I and II expiration nor that of post-inspiratory neurons during stage I expiration. Thus this depolarization probably resulted from synaptic excitation.(ABSTRACT TRUNCATED AT 250 WORDS)


This article has been cited by other articles:


Home page
 J. Neurophysiol.Home page
M. C. Bellingham
Synaptic Inhibition of Cat Phrenic Motoneurons by Internal Intercostal Nerve Stimulation
J Neurophysiol, September 1, 1999; 82(3): 1224 - 1232.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
J. E. Butler, D. K. McKenzie, A. R. Glanville, and S. C. Gandevia
Pulmonary Afferents Are Not Necessary for the Reflex Inhibition of Human Inspiratory Muscles Produced by Airway Occlusion
J Neurophysiol, July 1, 1997; 78(1): 170 - 176.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online