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Neuronal and glial metabolite content of the epileptogenic human hippocampus
Author(s) -
Petroff Ognen A. C.,
Errante Laura D.,
Rothman Douglas L.,
Kim Jung H.,
Spencer Dennis D.
Publication year - 2002
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.10360
Subject(s) - hippocampal formation , glutamate receptor , hippocampus , gliosis , epilepsy , glutamine , neuron , neuroscience , hippocampal sclerosis , endocrinology , medicine , temporal lobe , chemistry , biology , biochemistry , amino acid , receptor
Mesial temporal lobe epilepsy is characterized by hippocampal atrophy, hypometabolism, and decreased N ‐acetylaspartate, often attributed to neuron loss and gliosis. Twenty hippocampal specimens were obtained during temporal lobectomy and frozen quickly. Perchloric acid extracts of the small metabolites were analyzed by proton magnetic resonance spectroscopy. There were no significant associations between hippocampal neuron loss and the cellular content of N ‐acetylaspartate, glutamate, GABA, glutamine, or aspartate. The mean metabolite content of hippocampi with less than 30% of neurons remaining was the same as those with greater than 65% of neurons surviving. Mean N ‐acetylaspartate levels were below those reported by in vivo studies of control subjects. The highest and the lowest glutamate concentrations were seen in specimens with the worst neuron loss. A highly significant association between hippocampal N ‐acetylaspartate and glutamate content was seen with weak associations between N ‐acetylaspartate and aspartate and glutamate and aspartate. The hippocampal content of N ‐acetylaspartate, glutamate, GABA, glutamine, and aspartate is altered minimally by severe neuron loss in mesial temporal lobe epilepsy. The epileptic human hippocampus has increased intracellular glutamate content that may contribute to the epileptogenic nature of hippocampal sclerosis.