@article{ref1,
title="Serotonin2A/C receptors mediate the aggressive phenotype of TLX gene knockout mice",
journal="Behavioural brain research",
year="2013",
author="Juárez, Pablo and Valdovinos, Maria G. and May, Michael E. and Lloyd, Blair P. and Couppis, Maria H. and Kennedy, Craig H.",
volume="256",
number="",
pages="354-361",
abstract="Deleting the tailless (TLX) gene in mice produces a highly aggressive phenotype yet to be characterized in terms of heterozygous animals or neurotransmitter mechanisms. We sought to establish pharmacological control over aggression and study the role of serotonin (5-HT)2A/C receptors in mediating changes in aggression. We analyzed aggression in mice heterozygous (+/-) or homozygous (-/-) for the TLX gene and wild-types (+/+) using a resident-intruder paradigm. No +/+ mice were aggressive, 36% of +/- TLX and 100% of -/- TLX mice showed aggression. Dose-effect functions were established for clozapine (0.1-1.5mg/kg, ip), ketanserin (0.3-1.25mg/kg, ip), and (±)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane [(±)DOI] (0.5-2.0mg/kg, ip). Injecting clozapine decreased the frequency and duration of attacks for +/- TLX and -/- TLX mice. Clozapine did not decrease grooming in either +/- TLX or -/- TLX mice but may have increased locomotion for -/- TLX mice. Injecting ketanserin, a 5-HT2A/C receptor antagonist, produced differential decreases in frequency and latency to aggression between genotypes and corresponding increases in locomotor behavior. Injecting (±)DOI, a 5-HT2A/C receptor agonist, increased the frequency and duration of attacks, decreased the latency to attacks, and decreased locomotion in +/- and -/- TLX mice. Results of the current study suggest aggression displayed by TLX null and heterozygous mice involves 5-HT2A/C receptors.<p /> <p>Language: en</p>",
language="en",
issn="0166-4328",
doi="10.1016/j.bbr.2013.07.044",
url="http://dx.doi.org/10.1016/j.bbr.2013.07.044"
}