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Hippocampal N ‐acetyl aspartate levels do not mirror neuronal cell densities in creatine‐supplemented epileptic rats
Author(s) -
Vielhaber Stefan,
Kudin Alexei P.,
Kudina Tatiana A.,
Stiller Detlef,
Scheich Henning,
Schoenfeld Ariel,
Feistner Helmut,
Heinze HansJochen,
Elger Christian E.,
Kunz Wolfram S.
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02954.x
Subject(s) - hippocampal formation , creatine , neuroprotection , epilepsy , hippocampus , pilocarpine , in vivo , neuroscience , endocrinology , temporal lobe , medicine , creatine kinase , chemistry , biology , microbiology and biotechnology
For neuroprotective therapy of neurodegenerative diseases creatine treatment has gained special interest because creatine has been shown to cross the blood–brain barrier, accumulate in the human brain in vivo and cause delayed neuronal cell death in a large number of animal models. Here, we used the pilocarpine model of temporal lobe epilepsy to determine whether creatine administration is able to attenuate the epilepsy‐associated decrease in hippocampal N ‐acetyl aspartate (NAA) concentrations, impairment of mitochondrial function and neuronal cell loss. In vivo 1 H‐NMR spectroscopy showed, in epileptic rats after creatine administration, higher hippocampal NAA concentrations, suggesting improved neuronal survival. However, in vitro observation of hippocampal slices from creatine‐treated epileptic rats revealed a more pronounced loss of pyramidal neurons and decrease in activity of mitochondrial enzymes in hippocampal subfields. This indicates that NAA concentrations measured by in vivo 1 H‐NMR spectroscopy reflect alterations of metabolism rather than neuronal cell densities. Our data indicate an adverse effect of creatine on neuronal survival under conditions of enhanced neuronal activity.