Sleep Apneas are Increased in Mice Lacking Monoamine Oxidase A
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چکیده
منابع مشابه
Adaptive changes in postsynaptic dopamine receptors despite unaltered dopamine dynamics in mice lacking monoamine oxidase B.
Monoamine oxidase (MAO) B is considered a key enzyme in dopamine metabolism. The present studies, conducted in MAO B knockout mice, show that lack of MAO B does not alter extracellular levels of dopamine in striatum. Similarly, the synthesis, storage, uptake, and release of dopamine are also unaltered. However, autoradiography revealed a significant up-regulation of the D2-like dopamine recepto...
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The recent development of mice doubly deficient for monoamine oxidase A and B (MAO-A/B, respectively) has raised questions about the impact of these mutations on cardiovascular function, in so far as these animals demonstrate increased tissue levels of the vasoactive amines serotonin, norepinephrine, dopamine, and phenylethylamine. We recorded femoral arterial pressures and electrocardiograms i...
متن کاملMaladaptive defensive behaviours in monoamine oxidase A-deficient mice.
Rich evidence indicates that monoamine oxidase (MAO) A, the major enzyme catalysing the degradation of monoamine neurotransmitters, plays a key role in emotional regulation. Although MAOA deficiency is associated with reactive aggression in humans and mice, the involvement of this enzyme in defensive behaviour remains controversial and poorly understood. To address this issue, we tested MAOA kn...
متن کاملKnockout Corner : Knockout mice for monoamine oxidase A
A line of transgenic mice was isolated in which transgene integration had caused a deletion in the gene encoding monoamine oxidase A, an enzyme that degrades serotonin and norepinephrine. This has provided an animal model of MAOA deficiency in humans, a condition characterized by borderline mental retardation and impulsive aggression. Received 13 June 1999 ; Reviewed 14 June 1999 ; Accepted 16 ...
متن کاملKnockout Corner: Knockout mice for monoamine oxidase A.
A line of transgenic mice was isolated in which transgene integration had caused a deletion in the gene encoding monoamine oxidase A, an enzyme that degrades serotonin and norepinephrine. This has provided an animal model of MAOA deficiency in humans, a condition characterized by borderline mental retardation and impulsive aggression.
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ژورنال
عنوان ژورنال: Sleep
سال: 2007
ISSN: 1550-9109,0161-8105
DOI: 10.1093/sleep/30.10.1295