Catechol- <i>O</i> -methyltransferase-deficient mice exhibit sexually dimorphic changes in catecholamine levels and behavior
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- Joseph A. Gogos
- The Rockefeller University, New York, NY 10021; Columbia University, College of Physicians and Surgeons, Center for Neurobiology and Behavior, New York, NY 10032; and Hunter College, New York, NY 10021
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- Maria Morgan
- The Rockefeller University, New York, NY 10021; Columbia University, College of Physicians and Surgeons, Center for Neurobiology and Behavior, New York, NY 10032; and Hunter College, New York, NY 10021
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- Victoria Luine
- The Rockefeller University, New York, NY 10021; Columbia University, College of Physicians and Surgeons, Center for Neurobiology and Behavior, New York, NY 10032; and Hunter College, New York, NY 10021
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- Miklos Santha
- The Rockefeller University, New York, NY 10021; Columbia University, College of Physicians and Surgeons, Center for Neurobiology and Behavior, New York, NY 10032; and Hunter College, New York, NY 10021
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- Sonoko Ogawa
- The Rockefeller University, New York, NY 10021; Columbia University, College of Physicians and Surgeons, Center for Neurobiology and Behavior, New York, NY 10032; and Hunter College, New York, NY 10021
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- Donald Pfaff
- The Rockefeller University, New York, NY 10021; Columbia University, College of Physicians and Surgeons, Center for Neurobiology and Behavior, New York, NY 10032; and Hunter College, New York, NY 10021
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- Maria Karayiorgou
- The Rockefeller University, New York, NY 10021; Columbia University, College of Physicians and Surgeons, Center for Neurobiology and Behavior, New York, NY 10032; and Hunter College, New York, NY 10021
説明
<jats:p> Catechol- <jats:italic>O</jats:italic> -methyltransferase (COMT) is one of the major mammalian enzymes involved in the metabolic degradation of catecholamines and is considered a candidate for several psychiatric disorders and symptoms, including the psychopathology associated with the 22q11 microdeletion syndrome. By means of homologous recombination in embryonic stem cells, a strain of mice in which the gene encoding the COMT enzyme has been disrupted was produced. The basal concentrations of brain catecholamines were measured in the striatum, frontal cortex, and hypothalamus of adult male and female mutants. Locomotor activity, anxiety-like behaviors, sensorimotor gating, and aggressive behavior also were analyzed. Mutant mice demonstrated sexually dimorphic and region-specific changes of dopamine levels, notably in the frontal cortex. In addition, homozygous COMT-deficient female (but not male) mice displayed impairment in emotional reactivity in the dark/light exploratory model of anxiety. Furthermore, heterozygous COMT-deficient male mice exhibited increased aggressive behavior. Our results provide conclusive evidence for an important sex- and region-specific contribution of COMT in the maintenance of steady-state levels of catecholamines in the brain and suggest a role for COMT in some aspects of emotional and social behavior in mice. </jats:p>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 95 (17), 9991-9996, 1998-08-18
Proceedings of the National Academy of Sciences
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詳細情報 詳細情報について
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- CRID
- 1360855570257869184
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- NII論文ID
- 80010583655
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- ISSN
- 10916490
- 00278424
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- データソース種別
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