Abstract

Our social relationships determine our health and well-being. In rodent models, there is now strong support for the rewarding properties of aggressive or assertive behaviors to be critical for the expression and development of adaptive social relationships, buffering from stress and protecting from the development of psychiatric disorders such as depression. However, due to the false belief that aggression is not a part of the normal repertoire of social behaviors displayed by females, almost nothing is known about the neural mechanisms mediating the rewarding properties of aggression in half the population. In the following study, using Syrian hamsters as a well-validated and translational model of female aggression, we investigated the effects of aggressive experience on the expression of markers of postsynaptic structure (PSD-95, Caskin I) and excitatory synaptic transmission (GluA1, GluA2, GluA4, NR2A, NR2B, mGluR1a, and mGluR5) in the nucleus accumbens (NAc), caudate putamen and prefrontal cortex. Aggressive experience resulted in an increase in PSD-95, GluA1 and the dimer form of mGluR5 specifically in the NAc 24 h following aggressive experience. There was also an increase in the dimer form of mGluR1a 1 week following aggressive experience. Aggressive experience also resulted in an increase in the strength of the association between these postsynaptic proteins and glutamate receptors, supporting a common mechanism of action. In addition, 1 week following aggressive experience there was a positive correlation between the monomer of mGluR5 and multiple AMPAR and NMDAR subunits. In conclusion, we provide evidence that aggressive experience in females results in an increase in the expression of postsynaptic density, AMPARs and group I metabotropic glutamate receptors, and an increase in the strength of the association between postsynaptic proteins and glutamate receptors. This suggests that aggressive experience may result in an increase in excitatory synaptic transmission in the NAc, potentially encoding the rewarding and behavioral effects of aggressive interactions.

Highlights

  • One in five adults in the United States suffer from a diagnosable mental disorder, such as depression, schizophrenia, anxiety disorder, and autism spectrum disorder (National Institute of Mental Health website: statistics)

  • To begin to develop this line of research, we investigated the effects of female aggressive experience on the expression of proteins associated with postsynaptic plasticity (PSD-95 and Caskin I) and excitatory synaptic transmission, AMPARs (GluA1, GluA2, and GluA4), NMDARs (NR2A and NR2B) and group I mGluRs (Gq-protein coupled monomer and dimer forms of mGluR1a and mGluR5) in the nucleus accumbens (NAc)

  • To gain insight into potential mechanisms mediating changes in postsynaptic density and excitatory synaptic transmission, we investigated the strength of associations between the various postsynaptic structure proteins and glutamate receptors analyzed, and potential effects of aggressive experience on these relationships

Read more

Summary

Introduction

The pervasive expression of agonistic encounters, dominant-subordinate relationships, and social hierarchies across the animal kingdom is evidence of the beneficial, adaptive and rewarding properties of aggression (Meisel and Joppa, 1994; Abbott et al, 1998; Edwards and Spitzer, 2006; Pettinger et al, 2011; Albers, 2012; Gil et al, 2013) These adaptive processes are critical for resource allocation, reproductive success and survival for males and females (Digby and McLean Stevens, 2007; Nelson and Trainor, 2007; Lindenfors and Tullberg, 2011; Stockley and Bro-Jorgensen, 2011; Giebel et al, 2013)

Objectives
Methods
Results
Conclusion

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.