Document Detail


Hippocampal extracellular GABA correlates with metabolism in human epilepsy.
MedLine Citation:
PMID:  18807158     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
As the major inhibitory neurotransmitter in human brain, GABA is an important modulator of hyperexcitability in epilepsy patients. Given the high energetic cost of neurotransmission and synaptic activity, GABA concentrations may be hypothesized to correlate with metabolic function. We studied human epilepsy patients undergoing intracranial EEG monitoring for seizure localization to examine microdialysis measures of extracellular GABA (ecGABA), pre-operative MR spectroscopic measures of neuronal mitochondrial function (NAA/Cr), and wherever possible, neuropathology and hippocampal volumetry. Two groups undergoing intracranial monitoring for seizure localization were studied: surgically treated hippocampal epilepsy (MTLE) and neocortical (non-hippocampal seizure onset) epilepsy. All data are hippocampal and thus these groups allow comparisons between the epileptogenic and non-epileptogenic regions. ecGABA was measured using in vivo microdialysis performed during intracranial monitoring. Pre-operative in vivo MR spectroscopic imaging was performed to measure the ratio of N-acetyl aspartate (NAA) to creatine. Standard methods for neuropathology and hippocampal volumetry were used. In the neocortical group, increased ecGABA correlated with greater NAA/Cr (R = +0.70, p < 0.015, n = 12) while in the MTLE group, increased ecGABA linked with decreased NAA/Cr (R = -0.94, p < 0.001, n = 8). In MTLE, ecGABA (increased) and NAA/Cr (decreased) correlated with increased glial cell numbers (R = +0.71, p < 0.01, n = 12, R = -0.76 p < 0.03 respectively). No relationship was seen between ecGABA and hippocampal volumes in either group. In epilepsy, ecGABA increases occur across a range of metabolic function. Outside the seizure focus, ecGABA and NAA/Cr increase together; in contrast, within the seizure focus, ecGABA increases with declining mitochondrial function.
Authors:
J W Pan; I Cavus; J Kim; H P Hetherington; D D Spencer
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2008-09-18
Journal Detail:
Title:  Metabolic brain disease     Volume:  23     ISSN:  0885-7490     ISO Abbreviation:  Metab Brain Dis     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-10-29     Completed Date:  2009-01-09     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  8610370     Medline TA:  Metab Brain Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  457-68     Citation Subset:  IM    
Affiliation:
Department of Neurosurgery, Yale University School of Medicine, New Haven, CT, 06520, USA. jullie.pan@yale.edu
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Case-Control Studies
Energy Metabolism / physiology*
Epilepsy / metabolism*
Female
Hippocampus / metabolism*
Humans
Magnetic Resonance Spectroscopy
Male
Matched-Pair Analysis
Microdialysis
Middle Aged
Mitochondria / metabolism
Reference Values
Young Adult
gamma-Aminobutyric Acid / metabolism*
Grant Support
ID/Acronym/Agency:
AT02984/AT/NCCAM NIH HHS; EB00473/EB/NIBIB NIH HHS; NS054038/NS/NINDS NIH HHS; R01 NS040550/NS/NINDS NIH HHS; R21 AT002984/AT/NCCAM NIH HHS; R21 DK064565/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
56-12-2/gamma-Aminobutyric Acid
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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