Identification of Quantitative Trait Loci That Affect Aggressive Behavior in Mice

Brodkin, Edward S.; Goforth, Sarah A.; Keene, Angela H.; Fossella, John; Silver, Lee M.

doi:10.1523/jneurosci.22-03-01165.2002

Cited by 81 publications

(72 citation statements)

References 36 publications

(42 reference statements)

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“…Intriguingly, Guillot and Chapouthier (1996) have found that males of more aggressive strains are also more anxious. Unfortunately, Guillot and Chapouthier (1996) did not test males from the A/J strain and it is well known that A/J mice are markedly unaggressive (Brodkin et al 2002). It can be concluded that if there is a relationship between intermale aggression and anxiety-related behavior it is certainly not a simple one.…”

Section: Discussionmentioning

confidence: 99%

Chromosomal Assignment of Quantitative Trait Loci Influencing Modified Hole Board Behavior in Laboratory Mice using Consomic Strains, with Special Reference to Anxiety-related Behavior and Mouse Chromosome 19

2008

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Male mice from a panel of chromosome substitution strains (CSS, also called consomic strains or lines)-in which a single full-length chromosome from the A/J inbred strain has been transferred onto the genetic background of the C57BL/6J inbred strain-and the parental strains were examined in the modified hole board test. This behavioral test allows to assess for a variety of different motivational systems in parallel (i.e. anxiety, risk assessment, exploration, memory, locomotion, and arousal). Such an approach is essential for behavioral characterization since the motivational system of interest is strongly influenced by other behavioral systems. Both univariate and bivariate analyses, as well as a factor analysis, were performed. The C57BL/6J and A/J mouse parental inbred strains differed in all motivational systems. The chromosome substitution strain survey indicated that nearly all mouse chromosomes (with the exception of chromosome 2) each contain at least one quantitative trait locus (QTL) that is involved in modified hole board behavior. The results agreed well with previous reports of QTLs for anxiety-related behavior using the A/J and

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Section: Discussionmentioning

confidence: 99%

Chromosomal Assignment of Quantitative Trait Loci Influencing Modified Hole Board Behavior in Laboratory Mice using Consomic Strains, with Special Reference to Anxiety-related Behavior and Mouse Chromosome 19

2008

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“…These suggestions are also consistent with the reported involvement of MAP kinase pathways in the regulation of several neurotransmitter systems (Della Rocca et al, 1999;Greengard, 2001) that have been implicated in the regulation of aggressivity. These include serotonergic (Birger et al, 2003;Davidge et al, 2004;Edwards and Kravitz, 1997;Ferris et al, 1999;Huber et al, 1997;Korte et al, 1996;Manuck et al, 2002;Miczek et al, 2001), dopamine, norepinephrine, GABA, glutamate, acetylcholine, cholecystokinin, substance P, and opioid neurotransmitter systems (Brodkin et al, 2002;Chiavegatto et al, 2001;Olivier et al, 1995;Siegel et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Methamphetamine Causes Alterations in the MAP Kinase-Related Pathways in the Brains of Mice that Display Increased Aggressiveness

Sokolov

Cadet

2005

Neuropsychopharmacol

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Aggressive behaviors have been reported in patients who suffer from some psychiatric disorders, and are common in methamphetamine (METH) abusers. Herein, we report that multiple (but not single) injections of METH significantly increased aggressiveness in male CD-1 mice. This increase in aggressiveness was not secondary to METH-induced hyperactivity. Analysis of protein expression using antibody microarrays and Western blotting revealed differential changes in MAP kinase-related pathways after multiple and single METH injections. There were statistically significant (po0.05) decreases in MEK1, Erk2p, GSK3a, 14-3-3e, and MEK7 in the striata of mice after multiple injections of METH. MEK1 was significantly decreased also after a single injection of METH, but to a much lesser degree than after multiple injections of METH. In the frontal cortex, there was a statistically significant decrease in GSK3a after multiple (but not single) injections of METH. These findings suggest that alterations in MAP kinase-related pathways in the prefronto-striatal circuitries might be involved in the manifestation of aggressive behaviors in mice. Neuropsychopharmacology (2006) 31, 956-966.

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“…For example, Brodkin et al [10], using an outcross-backcross protocol and genome-wide scan discovered aggression quantitative trait loci on distal chromosome 10 and proximal chromosome X. Of further significance, these authors suggested that the diacylglycerol kinase alpha subunit gene (Dagk1) and the glutamate receptor subunit AMPA3 gene (Gria3) are candidate genes for aggressive behavior.…”

Section: Genetic Studiesmentioning

confidence: 99%

The Neurobiological Bases for Development of Pharmacological Treatments of Aggressive Disorders

Siegel

Bhatt²,

Bhatt³

et al. 2007

123

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Violence and aggression are major causes of death and injury, thus constituting primary public health problems throughout much of the world costing billions of dollars to society. The present review relates our understanding of the neurobiology of aggression and rage to pharmacological treatment strategies that have been utilized and those which may be applied in the future. Knowledge of the neural mechanisms governing aggression and rage is derived from studies in cat and rodents. The primary brain structures involved in the expression of rage behavior include the hypothalamus and midbrain periaqueductal gray. Limbic structures, which include amygdala, hippocampal formation, septal area, prefrontal cortex and anterior cingulate gyrus serve important modulating functions. Excitatory neurotransmitters that potentiate rage behavior include excitatory amino acids, substance P, catecholamines, cholecystokinin, vasopressin, and serotonin that act through 5-HT2 receptors. Inhibitory neurotransmitters include GABA, enkephalins, and serotonin that act through 5-HT1 receptors. Recent studies have demonstrated that brain cytokines, including IL-1 and IL-2, powerfully modulate rage behavior. IL-1 exerts its actions by acting through 5-HT2 receptors, while IL-2 acts through GABAA or NK1 receptors. Pharmacological treatment strategies utilized for control of violent behavior have met with varying degrees of success. The most common approach has been to apply serotonergic compounds. Others included the application of antipsychotic, GABAergic (anti-epileptic) and dopaminergic drugs. Present and futures studies on the neurobiology of aggression may provide the basis for new and novel treatment strategies for the control of aggression and violence as well as the continuation of existing pharmacological approaches.

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Identification of Quantitative Trait Loci That Affect Aggressive Behavior in Mice

Cited by 81 publications

References 36 publications

Chromosomal Assignment of Quantitative Trait Loci Influencing Modified Hole Board Behavior in Laboratory Mice using Consomic Strains, with Special Reference to Anxiety-related Behavior and Mouse Chromosome 19

Chromosomal Assignment of Quantitative Trait Loci Influencing Modified Hole Board Behavior in Laboratory Mice using Consomic Strains, with Special Reference to Anxiety-related Behavior and Mouse Chromosome 19

Methamphetamine Causes Alterations in the MAP Kinase-Related Pathways in the Brains of Mice that Display Increased Aggressiveness

The Neurobiological Bases for Development of Pharmacological Treatments of Aggressive Disorders

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