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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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Antipsychotics for aggression in adults: A meta-analysis

TL;DR: Although antipsychotics appear to be effective for treatment of aggression, their small effect sizes in the context of their significant side‐effects should be taken into account when making clinical decisions about their use.
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Relationship between imidazoline/guanidinium receptive sites and monoamine oxidase A and B.

TL;DR: Allosteric regulation of the activity of MAO via the imidazoline binding domains may be of significance in various disease states associated with elevated enzyme expression or in which the enzyme is a therapeutic target.
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Modulation of agonist and antagonist interactions in serotonin 1A receptors by alcohols.

TL;DR: The results show that alcohols inhibit the specific binding of the agonist OH‐DPAT and the antagonist p‐MPPF to 5‐HT1A receptors in a concentration‐dependent manner.
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Impairment of social behaviors in Arhgef10 knockout mice

TL;DR: The results suggest that ARHGEF10 is a candidate risk gene for ASD and that the Arhgef10 knockout model could be a tool for studying the mechanisms of neurotransmission in ASD.
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Synthesis and biological evaluation of enantiomerically pure 3-(1H-Pyrrol-1-yl)-2-oxazolidinones as a new class of potent and selective monoamine oxidase type A inhibitors

TL;DR: Based on searches on CNS potentially active compounds containing a pyrrole moiety, 3-(1H-pyrrol-1-yl)-2-oxazolidinones and isomeric 3-3-yl-2-and-yl -2-Oxazolid inones were prepared as anti-MAO agents and resulted selective and reversible MAO-A inhibitors.
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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