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Aggressive Behavior and Altered Amounts of Brain Serotonin and Norepinephrine in Mice Lacking MAOA

TLDR
Pup behavioral alterations, including trembling, difficulty in righting, and fearfulness were reversed by the serotonin synthesis inhibitor parachlorophenylalanine, and adults manifested a distinct behavioral syndrome, including enhanced aggression in males.
Abstract
Deficiency in monoamine oxidase A (MAOA), an enzyme that degrades serotonin and norepinephrine, has recently been shown to be associated with aggressive behavior in men of a Dutch family. A line of transgenic mice was isolated in which transgene integration caused a deletion in the gene encoding MAOA, providing an animal model of MAOA deficiency. In pup brains, serotonin concentrations were increased up to ninefold, and serotonin-like immunoreactivity was present in catecholaminergic neurons. In pup and adult brains, norepinephrine concentrations were increased up to twofold, and cytoarchitectural changes were observed in the somatosensory cortex. Pup behavioral alterations, including trembling, difficulty in righting, and fearfulness were reversed by the serotonin synthesis inhibitor parachlorophenylalanine. Adults manifested a distinct behavioral syndrome, including enhanced aggression in males.

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Effect of Monoamine Oxidase Gene Knockout on Dopamine Metabolism in Mouse Brain Structures

TL;DR: The results suggest that monoamine oxidases A and B and catechol-O-methyltransferase play different roles in dopamine metabolism in various brain structures.
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MAOA variants differ in oscillatory EEG & ECG activities in response to aggression-inducing stimuli

TL;DR: The electroencephalogram and electrocardiogram results obtained under aggression-related stimulation revealed oscillatory changes as novel phenotypes that vary with the MAOA genotype, providing genetic insights into MAOA function and offer a neurobiological basis for various socio-emotional mechanisms in healthy individuals.
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Behavior and gene expression in the brain of adult self-fertilizing mangrove rivulus fish (Kryptolebias marmoratus) after early life exposure to the neurotoxin β-N-methylamino-l-alanine (BMAA)

TL;DR: It is revealed that BMAA can have long-lasting effects on the brain that are suspected to affect phenotypic traits with aging and highlights the importance of studying delayed effects in ecotoxicological studies.

Roles of forced nicotine exposure and Comt gene disruption in the development of addiction-related behavioural and neurochemical changes in mice

TL;DR: In this article, the authors propose a solution to solve the problem of concurrence of the 2.7.7 dB.0 dB.1 dB.2 dB.5 dB.
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Interactions between MAOA and SYP polymorphisms were associated with symptoms of attention-deficit/hyperactivity disorder in Chinese Han subjects

TL;DR: It is suggested that the interaction of MAOA and SYP may be involved in the genetic mechanism of ADHD‐I subtype and predict ADHD symptoms.
References
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Behavioral despair in mice: a primary screening test for antidepressants

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Functional role of type I and type II interferons in antiviral defense.

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The structural organization of layer IV in the somatosensory region (SI) of mouse cerebral cortex. The description of a cortical field composed of discrete cytoarchitectonic units.

TL;DR: The author describes how his methods of investigation with celloidin embedded material prepared with the Golgi method and Nissl staining revealed for the first time the “barrel fields” of the mouse cerebral cortex that are activated by stimulation of the facial vibrissae (whiskers).
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Genetic Applications of an Inverse Polymerase Chain Reaction

TL;DR: The feasibility of IPCR is shown by amplifying the sequences that flank an IS1 element in the genome of a natural isolate of Escherichia coli.
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Abnormal behavior associated with a point mutation in the structural gene for monoamine oxidase A

TL;DR: Analytical results indicate that isolated complete MAOA deficiency in this family is associated with a recognizable behavioral phenotype that includes disturbed regulation of impulsive aggression.
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