JN Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Neurophysiol 92: 1011-1022, 2004. First published March 31, 2004; doi:10.1152/jn.00110.2004
0022-3077/04 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
92/2/1011    most recent
00110.2004v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
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 ISI Web of Science (3)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nita, D. A.
Right arrow Articles by Amzica, F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nita, D. A.
Right arrow Articles by Amzica, F.

Nonneuronal Origin of CO2-Related DC EEG Shifts: An In Vivo Study in the Cat

Dragos A. Nita1, Sampsa Vanhatalo2, Frantz-Daniel Lafortune1, Juha Voipio2, Kai Kaila2 and Florin Amzica1

1Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Quebec G1K 7P4, Canada; and 2Laboratory of Neurobiology, Department of Biosciences, University of Helsinki, FIN-00014 Helsinki, Finland

Submitted 3 February 2004; accepted in final form 24 March 2004

We studied the mechanisms underlying CO2-dependent DC potential shifts, using epicranial, epidural, epicortical, intraventricular, and intraparenchymal (intraneuronal, intraglial, and field) recordings in ketamine–xylazine-anesthetized cats. DC shifts were elicited by changes in artificial ventilation, causing end-tidal CO2 variations within a 2–5% range. Hypercapnia was consistently associated with negative scalp DC shifts (average shift –284.4 µV/CO2%, range –216 to –324 µV/CO2%), whereas hypocapnia induced positive scalp DC shifts (average shift 307.8 µV/CO2%, range 234 to 342 µV/CO2%) in all electrodes referenced versus the nasium bone. The former condition markedly increased intracranial pressure (ICP), whereas the latter only slightly reduced ICP. Breakdown of the blood–brain barrier (BBB) resulted in a positive DC shift and drastically reduced subsequent DC responses to hypo-/hypercapnia. Thiopental and isoflurane also elicited a dose-dependent positive DC shift and, at higher doses, hypo-/hypercapnia responses displayed reverted polarity. As to the possible implication of neurons in the production of DC shifts, no polarity reversal was recorded between scalp, various intracortical layers, and deep brain structures. Moreover, the membrane potential of neurons and glia did not show either significant or systematic variations in association with the scalp-recorded CO2-dependent DC shifts. Pathological activities of neurons during spike-wave seizures produced DC shifts of significantly smaller amplitude than those generated by hyper-/hypocapnia. DC shifts were still elicited when neuronal circuits were silent during anesthesia-induced burst-suppression patterns. We suggest that potentials generated by the BBB are the major source of epicortical/cranial DC shifts recorded under conditions affecting brain pH and/or cerebral blood flow.


Address for reprint requests and other correspondence: F. Amzica, Laboratoire de Neurophysiologie, Faculté de Médecine, Université Laval, Quebec G1K 7P4, Canada (E-mail: florin.amzica{at}phs.ulaval.ca).




This article has been cited by other articles:


Home page
Anesth. Analg.Home page
H. Yoshida, T. Kushikata, S. Kabara, H. Takase, H. Ishihara, and K. Hirota
Flat Electroencephalogram Caused by Carbon Dioxide Pneumoperitoneum
Anesth. Analg., December 1, 2007; 105(6): 1749 - 1752.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2004 by the The American Physiological Society.