The Role of Brain Serotonin in the Expression of Genetically Determined Defensive Behavior

The Role of Brain Serotonin in the Expression of Genetically Determined Defensive Behavior The review summarizes the results of long-term studies on the role of the brain neurotransmitter serotonin in genetic predisposition to various types of defensive behavior. The involvement of the serotonergic brain system in the mechanisms of genetic control of both active and passive defensive responses has been established using silver foxes, Norway rats of S40 selection for low and high aggressiveness to humans, aggressive mice with genetic knockout of monoaminoxidase A, and S40 rats selected for predisposition to passive defensive response of freezing (catalepsy). The changes in the serotonergic 5-HT1A brain receptors of rats genetically predisposed to different strategies of defensive behavior were similar. However, the activity of the key enzyme of serotonin biosynthesis and the brain structures, in which serotonin metabolism was altered, significantly differed with regard to the preferred strategy. The conclusion was drawn that the 5-HT1A receptors and enzymes of serotonin metabolism in the brain are involved in implementing genetic control of defensive behavior. Expression of the 5-HT1A brain receptors was suggested to determine the levels of fear and anxiety and, consequently, the predisposition to defensive behavior, whereas the preferred strategy of defensive response (active or passive defensive) depends on genetically determined features of serotonin metabolism in the brain structures. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Russian Journal of Genetics Springer Journals

The Role of Brain Serotonin in the Expression of Genetically Determined Defensive Behavior

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Publisher
Kluwer Academic Publishers-Plenum Publishers
Copyright
Copyright © 2004 by MAIK “Nauka/Interperiodica”
Subject
Biomedicine; Human Genetics
ISSN
1022-7954
eISSN
1608-3369
D.O.I.
10.1023/B:RUGE.0000033309.92155.5a
Publisher site
See Article on Publisher Site

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