CJA
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text (PDF)
Right arrow Submit a scholarly reply
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by MORRIS, M. E.
Right arrow Search for Related Content
PubMed
Right arrow Articles by MORRIS, M. E.

Canadian Journal of Anesthesia, Vol 16, 494-507, Copyright © 1969 by Canadian Anesthesiologists' Society

The Effects of Respiratory Acidosis on a Sensory Relay System

MARY E. MORRIS M.D.1

1 Department of Research in Anaesthesia, McGill University, Montreal

The effects of hypercarbia on afferent inputs and synaptic transmission in the cuneate nucleus were studied in decerebrate cats. Stimulation with microelectrodes placed in the cuneate nucleus and/or dorsal column evoked antidromic potentials in the superficial radial nerve; stimulation of afferent fibres in the forelimb, dorsal column, or cuneate nucleus evoked orthodromic responses in the medial lemniscus. Small increases of inspired CO2 (<=5%) often increased synaptic transmission and the excitability of afferent fibres. Further increases of Pco2 depressed transmission and terminal excitability, while producing considerably smaller changes in postsynaptic excitability. CO2 had no obvious effect on the inhibition of orthodromic transmission produced by afferent nerve interaction, but markedly depressed the dorsal column reflexes. The efficiency of synaptic transmission, as estimated from the input-output relation of the cuneate, was maintained at individual active synapses. It is suggested that CO2 does not depress release of transmitter at this synapse, and that the changes in transmission are effected mainly by presynaptic events, possibly by block of conduction in the intraspinal afferent fibres and/or their terminals.

Note:

Supported by the Medical Research Council.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1969 by the Canadian Anesthesiologists' Society.