PMID- 36674893
OWN - NLM
STAT- MEDLINE
DCOM- 20230124
LR  - 20230201
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 24
IP  - 2
DP  - 2023 Jan 10
TI  - 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.
LID - 10.3390/ijms24021379 [doi]
LID - 1379
AB  - 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.
FAU - Borland, Johnathan M
AU  - Borland JM
AD  - Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA.
FAU - Dempsey, Desarae A
AU  - Dempsey DA
AUID- ORCID: 0000-0003-4681-0108
AD  - Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA.
AD  - Stark Neurosciences Research Institute, Indiana University School of Medicine, 
      Indianapolis, IN 46202, USA.
FAU - Peyla, Anna C
AU  - Peyla AC
AD  - Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA.
FAU - Hall, Megan A L
AU  - Hall MAL
AD  - Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA.
FAU - Kohut-Jackson, Abigail L
AU  - Kohut-Jackson AL
AD  - Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA.
FAU - Mermelstein, Paul G
AU  - Mermelstein PG
AD  - Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA.
FAU - Meisel, Robert L
AU  - Meisel RL
AUID- ORCID: 0000-0002-4277-8377
AD  - Department of Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA.
LA  - eng
GR  - 1856724/National Science Foundation/
GR  - T32DA007234/National Institute of Drug Abuse/
PT  - Journal Article
DEP - 20230110
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Cricetinae
MH  - Animals
MH  - Female
MH  - *Nucleus Accumbens/metabolism
MH  - Mesocricetus
MH  - Phosphorylation
MH  - *MAP Kinase Signaling System
MH  - Aggression/physiology
MH  - Prefrontal Cortex/metabolism
MH  - TOR Serine-Threonine Kinases/metabolism
PMC - PMC9862940
OTO - NOTNLM
OT  - caudate putamen
OT  - dominance
OT  - fragile X mental retardation protein
OT  - glutamate
OT  - prefrontal cortex
OT  - reward
OT  - social interaction
OT  - synaptic plasticity
COIS- The authors report no biomedical financial interests or potential conflict of 
      interest.
EDAT- 2023/01/22 06:00
MHDA- 2023/01/25 06:00
PMCR- 2023/01/10
CRDT- 2023/01/21 01:27
PHST- 2022/10/20 00:00 [received]
PHST- 2022/12/22 00:00 [revised]
PHST- 2022/12/28 00:00 [accepted]
PHST- 2023/01/21 01:27 [entrez]
PHST- 2023/01/22 06:00 [pubmed]
PHST- 2023/01/25 06:00 [medline]
PHST- 2023/01/10 00:00 [pmc-release]
AID - ijms24021379 [pii]
AID - ijms-24-01379 [pii]
AID - 10.3390/ijms24021379 [doi]
PST - epublish
SO  - Int J Mol Sci. 2023 Jan 10;24(2):1379. doi: 10.3390/ijms24021379.