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Molecular implications of prolonged aggression experience: Th, Dat1, Snca and Bdnf gene expression in the ventral tegmental area of the victorious male mice

Natalia P. Bondar¹, Ul’yana A. Boyarskikh², Irina L. Kovalenko¹, Maxim L. Filipenko² & Natalia N. Kudryavtseva¹

Correspondence: (Login to view email address)

1. Institute of Cytology and Genetics SD RAS
2. Institute of Chemical Biology and Basic Medicine SD RAS

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Document Type:

Manuscript

Date:

Received 06 July 2008 03:58 UTC; Posted 10 July 2008

Subjects:

Molecular Cell Biology, Neuroscience

Tags:

• repeated
• aggression,
• Th,
• Dat1,
• Snca,
• Bdnf,
• mRNA,
• aggression
• deprivation,
• sensory
• contact
• model,
• mice

Abstract:

Th, Dat1, Snca and Bdnf were the genes whose mRNA levels in the ventral tegmental area of the midbrain were measured in male mice that were victorious in 20 daily agonistic interactions and in a group of such victorious mice that had later not been allowed to fight for 14 days. This experiment demonstrated increased Th, Dat1 and Snca but not Bdnf mRNA levels in the former group as compared to the controls. In the latter group, the expression of the Th and Dat1 genes was still enhanced, while the level of Snca mRNA did not differ from that in the controls. These findings suggest that positive fighting experience enhances the expression of the genes concerned with dopaminergic systems and this enhanced expression is preserved for a long time afterwards. Significant positive correlations were found between the level of aggression and Th and Snca mRNA levels in the winners.

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This document is licensed to the public under the Creative Commons Attribution 3.0 License

How to cite this document:

Bondar, Natalia P., Boyarskikh, Ul’yana A., Kovalenko, Irina L., Filipenko, Maxim L., and Kudryavtseva, Natalia . Molecular implications of prolonged aggression experience: Th, Dat1, Snca and Bdnf gene expression in the ventral tegmental area of the victorious male mice. Available from Nature Precedings <http://hdl.handle.net/10101/npre.2008.2042.1> (2008)

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