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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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Suicidal behavior: relationship between phenotype and serotonergic genotype.

TL;DR: The basis of suicidal behavior (SB) is complex and multifactorial. Numerous risk factors have been identified. as discussed by the authors, including genetic factors that predispose individuals to disorders of complex etiology.
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Altered regulation of the 5-HT system in the brain of MAO-A knock-out mice.

TL;DR: 5‐HT mechanisms in knock‐out mice (2‐month‐old) lacking MAO‐A are investigated, indicating that the enhancement of extracellular 5‐HT levels induces a down‐regulation of the 5‐ HT transporter, and a desensitization of 5-HT1A autoreceptors which allows the maintenance of tonic activity of 4‐HT neurons in the DRN.
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Cluster B personality disorders are associated with allelic variation of monoamine oxidase A activity.

TL;DR: The notion that allelic variation of MAOA activity contributes modestly to the balance of hyper- (impulsive-aggressive) and hyporeactive (anxious-depressive) traits is supported.
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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