Serotonergic modulation of social interactions in isolated male mice

Olivier, Berend; Mos, J.; Heyden, Jan Van der; Hartog, J.E. Den

doi:10.1007/bf00442239

Cited by 126 publications

(47 citation statements)

References 9 publications

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“…quently increasing its synaptic availability 26 , and so reduces the hunger and the alimentary ingestion in humans 27 and produces hipofagia in rats 28 .…”

Section: Figmentioning

confidence: 99%

Neonatal treatment with fluoxetine reduces depressive behavior induced by forced swim in adult rats

Mendes‐da‐Silva

Souza

Barreto-Medeiros

et al. 2002

Arq. Neuro-Psiquiatr.

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-Serotonin plays a role at the pathophysiology of depression in humans and in experimental models. The present study investigated the depressive behavior and the weigh evolution in adult rats (60 days) treated from the 1st to the 21st postnatal day with fluoxetine, a selective serotonin reuptake inhibitor (10 mg/kg, sc, daily). The depressive behavior was induced by the forced swim test ( PALAVRAS-CHAVE: depressão, serotonina, inibidor de recaptação da 5-HT, neurogênese.

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“…quently increasing its synaptic availability 26 , and so reduces the hunger and the alimentary ingestion in humans 27 and produces hipofagia in rats 28 .…”

Section: Figmentioning

confidence: 99%

Neonatal treatment with fluoxetine reduces depressive behavior induced by forced swim in adult rats

Mendes‐da‐Silva

Souza

Barreto-Medeiros

et al. 2002

Arq. Neuro-Psiquiatr.

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“…It has been repeatedly demonstrated, in multiple species, that some individuals are sensitive to the aggression-heightening effects of moderate doses of Alc, while most are not (Chance et al, 1973;Peeke et al, 1973;Miczek and O'Donnell, 1980;Lister and Hilakivi, 1988;Miczek et al, 1993Miczek et al, , 2004b. Although the neurobiological basis for the differential response to Alc is not yet known, there is compelling evidence for a significant role of the serotonin (5-HT) system in the modulation of impulsive aggressive behavior (Olivier et al, 1989;Olivier and Mos, 1992;Miczek et al, 2004a).…”

Section: Introductionmentioning

confidence: 99%

Escalated Aggression after Alcohol Drinking in Male Mice: Dorsal Raphé and Prefrontal Cortex Serotonin and 5-HT1B Receptors

Faccidomo

Bannai

Miczek

2008

Neuropsychopharmacol

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A significant minority of individuals engages in escalated levels of aggression after consuming moderate doses of alcohol (Alc). Neural modulation of escalated aggression involves altered levels of serotonin (5-HT) and the activity of 5-HT 1B receptors. The aim of these studies was to determine whether 5-HT 1B receptors in the dorsal raphé (DRN), orbitofrontal (OFC), and medial prefrontal (mPFC) cortex attenuate heightened aggression and regulate extracellular levels of 5-HT. Male mice were trained to self-administer Alc by performing an operant response that was reinforced with a delivery of 6% Alc. To identify Alc-heightened aggressors, each mouse was repeatedly tested for aggression after consuming either 1.0 g/kg Alc or H 2 O. Next, a cannula was implanted into either the DRN, OFC, or mPFC, and subsets of mice were tested for aggression after drinking either Alc or H 2 O prior to a microinjection of the 5-HT 1B agonist, CP-94,253. Additional mice were implanted with a microdialysis probe into the mPFC, through which CP-94,253 was perfused and samples were collected for 5-HT measurement. Approximately 60% of the mice were more aggressive after drinking Alc, confirming the aggression-heightening effects of 1.0 g/kg Alc. Infusion of 1 mg CP-94,253 into the DRN reduced both aggressive and motor behaviors. However, infusion of 1 mg CP-94,253 into the mPFC, but not the OFC, after Alc drinking, increased aggressive behavior. In the mPFC, reverse microdialysis of CP-94,253 increased extracellular levels of 5-HT; levels decreased immediately after the perfusion. This 5-HT increase was attenuated in self-administering mice. These results suggest that 5-HT 1B receptors in the mPFC may serve to selectively disinhibit aggressive behavior in mice with a history of Alc self-administration.

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“…For instance, a negative correlation exists between serotonin (5-hydroxytryptamine; 5-HT) metabolites and impulsive aggressiveness in humans (10)(11)(12) and rodents (13,14). Pharmacological manipulations that increase 5-HT neurotransmission decrease the severity of aggressiveness in humans (15) and reduce aggression in animal models (16,17). Studies with selective 5-HT receptor agonists and genetically engineered mice strongly implicate the 5-HT 1A , 5-HT 1B , or both receptor subtypes in aggression (18)(19)(20)(21)(22).…”

mentioning

confidence: 99%

Brain serotonin dysfunction accounts for aggression in male mice lacking neuronal nitric oxide synthase

Chiavegatto

Dawson

Mamounas

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

152

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Genetically engineered mice with targeted disruption of the neuronal nitric oxide synthase (nNOS) gene established the inhibitory role of nitric oxide (NO) in male impulsive aggressive behavior. This was later confirmed by using selective nNOS inhibitors in male wild-type mice. The molecular mechanisms accounting for the aggressive behavior caused by the lack of neuronally derived NO is not known. Recent studies suggest that central serotonergic neuronal circuits and particularly 5-HT1A and 5-HT1B receptors play a prominent role in the regulation of aggression. Accordingly, we investigated whether the aggressiveness caused by the lack of nNOS might be because of alterations in serotonergic function. We now demonstrate that the excessive aggressiveness and impulsiveness of nNOS knockout mice is caused by selective decrements in serotonin (5-HT) turnover and deficient 5-HT1A and 5-HT1B receptor function in brain regions regulating emotion. These results indicate an important role for NO in normal brain 5-HT function and may have significant implications for the treatment of psychiatric disorders characterized by aggressiveness and impulsivity.T he gene encoding neuronal nitric oxide synthase (nNOS) was disrupted and inactivated by homologous recombination to clarify the functional role of nitric oxide (NO) as a messenger molecule in the nervous system (1). Mice lacking the gene for nNOS (nNOS Ϫ/Ϫ ) exhibit a variety of abnormalities including enlargement of the stomach (1), hypertrophied urinary bladders (2), reduced parasympathetic tone (3), and nocturnal motor deficits (4). In addition, male nNOS Ϫ/Ϫ mice display dramatic increases in aggressive and sexual behavior (5). Pharmacological treatment of male wild-type (WT) mice with selective nNOS inhibitor also evokes an increase in impulsive aggressive behavior to the levels displayed by nNOS Ϫ/Ϫ mice (6), indicating that the aggressive behavior is caused by loss of neuronally derived NO and not developmental abnormalities. nNOS is enriched throughout the limbic system (7, 8), an area important in emotional and agonistic behaviors and thus nNOS-derived NO is appropriately positioned to play a prominent role in regulating impulsive and aggressive behavior. Despite the evidence which implicates neuron-derived NO in the modulation of aggressive behavior, the molecular mechanisms by which NO regulate aggression are not known. Plasma androgen concentrations can affect the display of aggressive behavior in male mice, but testosterone concentrations in nNOS Ϫ/Ϫ and WT mice are similar (9).Previous studies of the brain mechanisms underlying aggression reveal that central serotonergic neuronal circuits are prominent in the regulation of aggression. For instance, a negative correlation exists between serotonin (5-hydroxytryptamine; 5-HT) metabolites and impulsive aggressiveness in humans (10-12) and rodents (13,14). Pharmacological manipulations that increase 5-HT neurotransmission decrease the severity of aggressiveness in humans (15) and reduce aggression in animal models ...

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Serotonergic modulation of social interactions in isolated male mice

Cited by 126 publications

References 9 publications

Neonatal treatment with fluoxetine reduces depressive behavior induced by forced swim in adult rats

Neonatal treatment with fluoxetine reduces depressive behavior induced by forced swim in adult rats

Escalated Aggression after Alcohol Drinking in Male Mice: Dorsal Raphé and Prefrontal Cortex Serotonin and 5-HT1B Receptors

Brain serotonin dysfunction accounts for aggression in male mice lacking neuronal nitric oxide synthase

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