Abnormal Behavior Associated with a Point Mutation in the Structural Gene for Monoamine Oxidase A

Brunner, Han G.; Nelen, Marcel; Breakefield, Xandra O.; Ropers, Hans‐Hilger; Oost, B.A. van

doi:10.1126/science.8211186

Cited by 1,460 publications

(812 citation statements)

References 34 publications

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“…These findings are consistent with abnormal behavior in men of the Dutch family with heritable lack of MAO A, showing disproportionate to the provocation impulsive aggression in response to psychosocial stress [Brunner et al, 1993].…”

Section: Discussionsupporting

confidence: 85%

Effect of MAO A deficiency on different kinds of aggression and social investigation in mice

Vishnivetskaya

Skrinskaya

Seif

et al. 2006

Aggressive Behavior

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Monoamine oxidase A (MAO A) degrades serotonin, dopamine and noradrenaline, factors critically involved in the regulation of aggression. Different kinds of aggression were investigated in Tg8, a transgenic mouse strain lacking a functional MAO A gene. MAO A-deficient mice differ from wild-type C3H/HeJ (C3H) in terms of showing higher territorial, predatory and isolationinduced aggression. Tg8 demonstrated shorter latencies to cricket killing and to the first attack after 6 weeks isolation than C3H mice. In the resident-intruder paradigm, MAO A-lacking mice were more aggressive than C3H when tested as intruders. In contrast to C3H, attack in Tg8 mice did not depend on different aggressiveness of intruders of BALB/c, A/Sn and C3H strains. Tg8 mice displayed no increase in aggression but demonstrated reduced social investigation towards anesthetized, as well as towards juvenile BALB/c males. Thus, MAO A deficiency in Tg8 mice is accompanied by increased expression of different kinds of aggression, as well as by disruption of normal pattern of social interaction. Aggr. Behav. 33:1-6, 2007. r

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Section: Discussionsupporting

confidence: 85%

Effect of MAO A deficiency on different kinds of aggression and social investigation in mice

Vishnivetskaya

Skrinskaya

Seif

et al. 2006

Aggressive Behavior

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“…Aggression alleles per se (in other words, influencing aggression but nothing else) probably do not exist, but there are some alleles that have been associated with aggression or aggression-related disorders. 2 For example, a point mutation in the monoamine oxidase A gene (MAO-A is an enzyme that breaks down 5-HT, NE, and DA) was described in a Dutch family with borderline mental retardation and intermittent explosive aggression (Brunner, Nelen, van Zandvoort, et al, 1993;Brunner, Nelen, Breakefield, Ropers, & van Oost, 1993). Although this appears to be an extremely rare condition, recent studies have shown that polymorphisms in the MAO-A gene may also be important in the etiology of antisocial behavior, in combination with environmental factors such as exposure to maltreatment in childhood (Caspi et al, 2002).…”

Section: The 5-ht 1b Receptor and Serotonergic Genesmentioning

confidence: 99%

The evidence for a neurobiological model of childhood antisocial behavior.

Goozen¹,

Fairchild²,

Snoek³

et al. 2007

Psychological Bulletin

414

393

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Children with persistent antisocial and aggressive behavior are diagnosed as having disruptive behavior disorder. The authors review evidence that antisocial children, and especially those who persist with this behavior as they grow older, have a range of neurobiological characteristics. It is argued that serotonergic functioning and stress-regulating mechanisms are important in explaining individual differences in antisocial behavior. Moreover, low fear of punishment and physiological underactivity may predispose antisocial individuals to seek out stimulation or take risks and may help to explain poor conditioning and socialization. The authors propose a theoretical model highlighting the interplay between neurobiological deficits and cognitive and emotional functioning as mediators of the link between early adversity and antisocial behavior problems in childhood. Implications for intervention programs are discussed.

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“…Loss of function of MAOA caused by a deficiency in the MAOA gene or decreased activity of the enzyme caused by a MAOA promoter polymorphism is associated with violent, criminal, or impulsive behavior in humans (Brunner et al, 1993). MAOA knockout mice also showed increased aggressive behavior where the brain NE and serotonin concentrations were markedly increased (Cases et al, 1995;Daniel et al, 2001).…”

Section: Cumulative Revolution Numbers/12hrmentioning

confidence: 99%

Monoamine Oxidase A Activity and Norepinephrine Level in Hippocampus Determine Hyperwheel Running in SPORTS Rats

Miyamoto

Harada

Hara

et al. 2006

Neuropsychopharmacol

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An understanding of neurological mechanisms for wheel running by rodents, especially with high exercise activity, would be applicable to a strategy for promotion of exercise motivation in humans. One of several brain regions that are candidates for the regulation of physical exercise is the hippocampus. Here we examined the running activity of Spontaneously-Running-Tokushima-Shikoku (SPORTS) rat, a new animal model for high levels of wheel-running activity, and its relation with the hippocampal norepinephrine (NE) system including the levels of NE, adrenergic receptors, and degradation enzymes for monoamines. In the hippocampus of SPORTS rats, the level of NE in extracellular fluid was augmented, whereas the level in the homogenate of the whole tissue was decreased even for sedentary conditions. Elevated extracellular NE caused downregulation of a 2 -adrenergic receptors in the hippocampus of SPORTS rats. Local administration of a 2 -adrenergic receptor antagonist yohimbine, but not of a 2 -agonist clonidine, into the hippocampus suppressed high running activity in SPORTS rats. The protein expression and the activity levels of monoamine oxidase A (MAOA), a critical enzyme for the degradation of NE, were decreased in the hippocampus of SPORTS rats to increase extracellular NE level. Thus, inhibition of oxidase activity in normal Wistar rats markedly increased wheel-running activity. These results indicate that decreased MAOA activity, elevation of extracellular NE, and a 2 -adrenergic receptors in the hippocampus determine the neural basis of the psychological regulation of exercise behavior in SPORTS rats.

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Abnormal Behavior Associated with a Point Mutation in the Structural Gene for Monoamine Oxidase A

Cited by 1,460 publications

References 34 publications

Effect of MAO A deficiency on different kinds of aggression and social investigation in mice

Effect of MAO A deficiency on different kinds of aggression and social investigation in mice

The evidence for a neurobiological model of childhood antisocial behavior.

Monoamine Oxidase A Activity and Norepinephrine Level in Hippocampus Determine Hyperwheel Running in SPORTS Rats

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