Dopamine-glutamate abnormalities in the frontal cortex associated with the catechol-O-methyltransferase (COMT) in schizophrenia

被引:15
|
作者
Brisch, Ralf [1 ]
Bernstein, Hans-Gert [1 ]
Krell, Dieter [1 ]
Dobrowolny, Henrik [1 ]
Bielau, Hendrik [1 ,2 ]
Steiner, Johann [1 ]
Gos, Tomasz [1 ,3 ]
Funke, Sieglinde [1 ]
Stauch, Renate [1 ]
Knueppel, Sven [4 ]
Bogert, Bernhard [1 ]
机构
[1] Otto VonGuericke Univ Magdegurg, Dept Psychiat, D-39120 Magdeburg, Germany
[2] Magdeburg Hosp gGmbH, Dept Psychiat, D-39130 Magdeburg, Germany
[3] Med Univ Gdansk, Inst Forens Med, PL-80204 Gdansk, Poland
[4] Max Delbruck Ctr Mol Med MDC Berlin Buch, Dept Bioinformat, D-13125 Berlin, Germany
关键词
Catechol-O-methyltransferase (COMT); Catecholamine; Dopamine; Schizophrenia; Paraffin-embedded human brain sections; MESSENGER-RNA EXPRESSION; DORSOLATERAL PREFRONTAL CORTEX; GLIAL-NEURONAL INTERACTIONS; 22Q11 DELETION SYNDROME; MOOD DISORDERS; NEUROTRANSMITTER INTERACTIONS; ANTIPSYCHOTIC-DRUGS; AGGRESSIVE-BEHAVIOR; METHYL TRANSFERASE; ENZYME-ACTIVITY;
D O I
10.1016/j.brainres.2009.02.039
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Catechol-O-methyltransferase (COMT) plays an important role in brain catecholamine metabolism. Several studies point to the involvement of COMT in schizophrenia. We applied COMT immunohistochemistry to paraffin-embedded brain sections and assessed the cell density of COMT expressing glial cells and COMT expressing neurons in the gray matter of the frontal cortex of patients with schizophrenia compared with control subjects. We found a significantly increased cell density of COMT expressing glial cells (p=0.003), but an unchanged cell density of COMT expressing neurons (p=0.778) in the gray matter of the frontal cortex of patients with schizophrenia compared with control subjects. our study demonstrates that schizophrenia might involve increased COMT expression in glial cells in the frontal cortex, which might be associated with a neuronal-glial abnormality and a disturbed dopamine-glutamate interaction. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:166 / 175
页数:10
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