PURPOSE: In situ 1H-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 NA/Cr ratios is a reflection of KA-induced neuronal cell loss.
PURPOSE: In situ 1H-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/Crratios increased significantly during the ictal phase. During the postictal and interictal phases, the NA/Crratio decreased. There was a significant and prolonged increase of the lactate/Crratio 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 lactateratios may reflect increased cellular activity and metabolism resulting from KA excitotoxicity. Assuming that the changes in NA/Crratios are due to NAA increase, we speculate that an activation of the N-acetylaspartylglutamate (NAAG) dipeptidase pathway may explain the ictal increase in NA/Crratios. The late postictal decrease in NA/Crratios is a reflection of KA-induced neuronal cell loss.
Authors: R Neppl; C M Nguyen; W Bowen; T Al-Saadi; J Pallagi; G Morris; W Mueller; R Johnson; R Prost; S D Rand Journal: AJNR Am J Neuroradiol Date: 2001 Nov-Dec Impact factor: 3.825
Authors: Natalie M Zahr; Elena L Fasano Crawford; Oliver Hsu; Shara Vinco; Dirk Mayer; Torsten Rohlfing; Edith V Sullivan; Adolf Pfefferbaum Journal: Brain Res Date: 2009-08-26 Impact factor: 3.252