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The NR1 N ‐Methyl‐ d ‐Aspartate Subunit and Brain‐derived Neurotrophic Factor in Temporal Lobe Epilepsy Hippocampus: A Comparison of Patients with and without Coexisting Psychiatric Symptoms
Author(s) -
Toro Carla Tatiana,
Hallak Jaime E.,
Dunham Jason S.,
Leite João P.,
Sakamoto Américo C.,
Guarnieri Ricardo,
Fong Vivian,
Deakin John F. W.
Publication year - 2007
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.1528-1167.2007.01194.x
Subject(s) - psychosis , dysphoria , psychology , nmda receptor , temporal lobe , hippocampus , epilepsy , neurotrophic factors , dentate gyrus , brain derived neurotrophic factor , neuroscience , glutamate receptor , hippocampal formation , medicine , endocrinology , psychiatry , receptor , anxiety
SummaryPurpose: The glutamate N ‐methyl‐ d ‐aspartate (NMDA) receptor and the neurotrophin brain‐derived neurotrophic factor have been implicated in the pathophysiology of schizophrenia and depression. Since these psychiatric disorders are common in temporal lobe epilepsy (TLE), a comparison of TLE patients with and without coexisting psychiatric symptoms may be useful to unravel pathophysiologic mechanisms for psychosis or depression.Methods: We used immunoautoradiography to assess the NR1 NMDA receptor subunit and brain‐derived neurotrophic factor in resected TLE hippocampus.Results: No changes relative to comparison controls were found for TLE patients with schizophrenia‐like psychosis or depression. Increased NR1 was found in the dentate molecular layer in the dysphoria group and unmedicated depressed patients.Conclusions: An increase in NR1 protein in the dentate molecular layer suggests an upregulation of NMDA receptors in granule cells in TLE patients with dysphoria and depression. This finding is compatible with the theory that increased NMDA receptor function is involved in the pathogenesis of depression and that antidepressants may act by opposing this mechanism.