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Temporal Changes in Proton MRS Metabolites After Kainic Acid‐Induced Seizures in Rat Brain
Author(s) -
Najm I. M.,
Wang Y.,
Hong S. C.,
Luders H. O.,
Ng T. C.,
Comair Y. G.
Publication year - 1997
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.1997.tb01082.x
Subject(s) - kainic acid , neuroscience , epilepsy , medicine , psychology , glutamate receptor , receptor
Summary:Purpose : In situ 1 H‐magnetic resonance spectroscopy (MRS) was used to study temporal metabolic changes in a rat model of temporal lobe epilepsy (TLE) by using kainic acid (KA). Methods: Rat brains were scanned at the level of the hippocampal body for MRS measurements. Relative ratios of N‐ acetyl groups (NA: N‐acetylaspartate and N‐acetylaspartyl glutamate), choline, and lactate (Lac) over creatine (Cr) were calculated. Results: NA/Cr ratios increased significantly during the ictal phase. During the postictal and interictal phases, the NA/Cr ratio decreased. There was a significant and prolonged increase of the lactate/Cr ratio in the hippocampi of rats that started 1 h after the onset of KA‐induced seizure activity and persisted up to 24 h after the injection. The prolonged lactate/Cr increase in an area susceptible to neuronal damage (e.g., hippocampus) correlated with the onset of seizure activity but remained elevated thereafter. Conclusions: The ictal and early postictal increase in lactate ratios may reflect increased cellular activity and metabolism resulting from KA excitotoxicity. Assuming that the changes in NA/Cr ratios are due to NAA increase, we speculate that an activation of the N‐acetylaspartylglutamate (NAAG) dipeptidase pathway may explain the ictal increase in NA/Cr ratios. The late postictal decrease in NNCr ratios is a reflection of KA‐induced neuronal cell loss.