Skip Navigation



Brain Advance Access published online on February 23, 2005
Brain, doi:10.1093/brain/awh444
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
128/5/1199    most recent
awh444v1
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Williamson, A.
Right arrow Articles by Hetherington, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Williamson, A.
Right arrow Articles by Hetherington, H.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received May 13, 2004
Revised December 23, 2004
Accepted January 4, 2005

Article

Correlations between granule cell physiology and bioenergetics in human temporal lobe epilepsy

Anne Williamson 1*, Peter R. Patrylo 2, Jullie Pan 3, Dennis D. Spencer 1, and Hoby Hetherington 3

1 Department of Neurosurgery, Yale University School of Medicine, New Haven, CT, USA
2 Department of Physiology, Southern Illinois University School of Medicine, Carbondale, IL, USA
3 Albert Einstein College of Medicine, New York, NY, USA

* To whom correspondence should be addressed.
Anne Williamson, E-mail: anne.williamson{at}yale.edu


  Abstract

Summary Human temporal lobe epilepsy (TLE) is associated with bioenergetic abnormalities including decreased phosphocreatine (PCr) normalized to ATP. The physiological consequences of these metabolic alterations have not been established. We hypothesized that impaired bioenergetics would correlate with alterations in physiological functions under conditions that strongly activate neural metabolism. We correlated several physiological variables obtained from epileptic human dentate granule cells studied in slices with hippocampal PCr/ATP measured using in vivo magnetic resonance spectroscopy. The physiological variables included: the ability to fire multiple action potentials in response to single stimuli, the inhibitory postsynaptic potential (IPSP) conductance and the responses to a 10 Hz, 10 s stimulus train. We noted a significant negative correlation between the ability to fire multiple spikes in response to single synaptic stimulation and PCr/ATP (P < 0.03) and a positive correlation between the IPSP conductance and PCr/ATP (P < 0.05). Finally, there was a strong correlation between PCr/ATP and the recovery of the membrane potential following a stimulus train (P < 0.01), with low PCr/ATP being associated with prolonged recovery times. These data suggest that the bioenergetic impairment seen in this tissue is associated with specific changes in excitatory and inhibitory neuronal responses to synchronized synaptic inputs.

Keywords: dentate gyrus; phosphocreatine; 13P-MRS; slice physiology; temporal lobe epilepsy.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Proc. Natl. Acad. Sci. USAHome page
J. J. Laschet, I. Kurcewicz, F. Minier, S. Trottier, J. Khallou-Laschet, J. Louvel, S. Gigout, B. Turak, A. Biraben, J.-M. Scarabin, et al.
Dysfunction of GABAA receptor glycolysis-dependent modulation in human partial epilepsy
PNAS, February 27, 2007; 104(9): 3472 - 3477.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.