Aggression Results in the Phosphorylation of ERK1/2 in the Nucleus Accumbens and the Dephosphorylation of mTOR in the Medial Prefrontal Cortex in Female Syrian Hamsters

Johnathan Borland, Desarae A. Dempsey, Anna C. Peyla, Megan A.L. Hall, Abigail L. Kohut-Jackson, Paul G. Mermelstein, Robert L. Meisel

Research output: Contribution to journalArticlepeer-review

Abstract

Like many social behaviors, aggression can be rewarding, leading to behavioral plasticity. One outcome of reward-induced aggression is the long-term increase in the speed in which future aggression-based encounters is initiated. This form of aggression impacts dendritic structure and excitatory synaptic neurotransmission in the nucleus accumbens, a brain region well known to regulate motivated behaviors. Yet, little is known about the intracellular signaling mechanisms that drive these structural/functional changes and long-term changes in aggressive behavior. This study set out to further elucidate the intracellular signaling mechanisms regulating the plasticity in neurophysiology and behavior that underlie the rewarding consequences of aggressive interactions. Female Syrian hamsters experienced zero, two or five aggressive interactions and the phosphorylation of proteins in reward-associated regions was analyzed. We report that aggressive interactions result in a transient increase in the phosphorylation of extracellular-signal related kinase 1/2 (ERK1/2) in the nucleus accumbens. We also report that aggressive interactions result in a transient decrease in the phosphorylation of mammalian target of rapamycin (mTOR) in the medial prefrontal cortex, a major input structure to the nucleus accumbens. Thus, this study identifies ERK1/2 and mTOR as potential signaling pathways for regulating the long-term rewarding consequences of aggressive interactions. Furthermore, the recruitment profile of the ERK1/2 and the mTOR pathways are distinct in different brain regions.

Original languageEnglish (US)
Article number1379
JournalInternational journal of molecular sciences
Volume24
Issue number2
DOIs
StatePublished - Jan 2023

Bibliographical note

Funding Information:
Research presented here was supported by NSF IOS 1856724 to R.L.M., P.G.M. and J.M.B. was supported by the National Institute on Drug Abuse of the National Institutes of Health under Award Number T32DA007234 to P.G.M. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Science Foundation and National Institutes of Health.

Publisher Copyright:
© 2023 by the authors.

Keywords

  • caudate putamen
  • dominance
  • fragile X mental retardation protein
  • glutamate
  • prefrontal cortex
  • reward
  • social interaction
  • synaptic plasticity

PubMed: MeSH publication types

  • Journal Article

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