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Open AccessJournal ArticleDOI

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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"Warrior genes" and the disease of being Māori

TL;DR: Could those Māori who express the "warrior" gene be diagnosed as having a medical condition similar to those with diseases such as Brunner syndrome or Norrie disease, two diseases involved in the expression of abnormal MAO genes?
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Neuronal and behavioral plasticity: the role of serotonin and BDNF systems tandem.

TL;DR: 5-HT–BDNF cross-talk is a potential target for the treatment of various neurological diseases and understanding the function of the members of BDNF system in response to challenges of the environment and the interaction with different 5-HT receptors in health and disease will one day lead to new classes of drugs.
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Effects of genetic depletion of monoamines on somatosensory cortical development.

TL;DR: Results show that monoamines have no instructive effect per se on the formation of thalamocortical patterning in S1, however, monoamines appear to be essential for the normal cytoarchitectonic maturation of the granular and supragranular cortical layers (II-III).
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NMDARs Mediate the Role of Monoamine Oxidase A in Pathological Aggression

TL;DR: The findings suggest that the role of MAO A in pathological aggression may be mediated by changes in NMDAR subunit composition in the PFC, and point to a critical function of this receptor in the molecular bases of antisocial personality.
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Locomotor Network Maturation Is Transiently Delayed in the MAOA-Deficient Mouse

TL;DR: Both in vivo and in vitro results argue for a transient delay of locomotor network maturation in the Tg8 strain.
References
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Journal Article

Behavioral despair in mice: a primary screening test for antidepressants

TL;DR: The mouse procedure is more rapid and less costly than that with rats and is thus more suitable for the primary screening of antidepressant drugs, suggesting that the procedure is selectively sensitive to antidepressant treatments.
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Functional role of type I and type II interferons in antiviral defense.

TL;DR: Comparison of mice lacking either type I or type II IFN receptors showed that, at least in response to some viruses, both IFN systems are essential for antiviral defense and are functionally nonredundant.
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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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