scholarly journals Social dominance differentially alters gene expression in the medial prefrontal cortex without affecting adult hippocampal neurogenesis or stress and anxiety‐like behavior

2019 ◽  
Vol 33 (6) ◽  
pp. 6995-7008 ◽  
Author(s):  
Anna Pallé ◽  
Candela Zorzo ◽  
Valerie E. Luskey ◽  
Kerry R. Mcgreevy ◽  
Silvia Fernández ◽  
...  
2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Ksenia Musaelyan ◽  
Selin Yildizoglu ◽  
James Bozeman ◽  
Andrea Du Preez ◽  
Martin Egeland ◽  
...  

Abstract Adult hippocampal neurogenesis is involved in stress-related disorders such as depression, posttraumatic stress disorders, as well as in the mechanism of antidepressant effects. However, the molecular mechanisms involved in these associations remain to be fully explored. In this study, unpredictable chronic mild stress in mice resulted in a deficit in neuronal dendritic tree development and neuroblast migration in the hippocampal neurogenic niche. To investigate molecular pathways underlying neurogenesis alteration, genome-wide gene expression changes were assessed in the prefrontal cortex, hippocampus and the hypothalamus alongside neurogenesis changes. Cluster analysis showed that the transcriptomic signature of chronic stress is much more prominent in the prefrontal cortex compared to the hippocampus and the hypothalamus. Pathway analyses suggested huntingtin, leptin, myelin regulatory factor, methyl-CpG binding protein and brain-derived neurotrophic factor as the top predicted upstream regulators of transcriptomic changes in the prefrontal cortex. Involvement of the satiety regulating pathways (leptin) was corroborated by behavioural data showing increased food reward motivation in stressed mice. Behavioural and gene expression data also suggested circadian rhythm disruption and activation of circadian clock genes such as Period 2. Interestingly, most of these pathways have been previously shown to be involved in the regulation of adult hippocampal neurogenesis. It is possible that activation of these pathways in the prefrontal cortex by chronic stress indirectly affects neuronal differentiation and migration in the hippocampal neurogenic niche via reciprocal connections between the two brain areas.


2009 ◽  
Vol 20 (5) ◽  
pp. 1064-1070 ◽  
Author(s):  
Maarten Loos ◽  
Tommy Pattij ◽  
Mieke C. W. Janssen ◽  
Danielle S. Counotte ◽  
Anton N. M. Schoffelmeer ◽  
...  

2019 ◽  
Vol 236 (12) ◽  
pp. 3525-3539 ◽  
Author(s):  
Bruno G. Berardino ◽  
Estefanía A. Fesser ◽  
Laura M. Belluscio ◽  
Octavio Gianatiempo ◽  
Nicolás Pregi ◽  
...  

Heliyon ◽  
2016 ◽  
Vol 2 (12) ◽  
pp. e00222 ◽  
Author(s):  
Shigeo Miyata ◽  
Masashi Kurachi ◽  
Noriko Sakurai ◽  
Yuchio Yanagawa ◽  
Yasuki Ishizaki ◽  
...  

2016 ◽  
Vol 113 (45) ◽  
pp. E7097-E7105 ◽  
Author(s):  
Hirobumi Tada ◽  
Tomoyuki Miyazaki ◽  
Kiwamu Takemoto ◽  
Kenkichi Takase ◽  
Susumu Jitsuki ◽  
...  

Social separation early in life can lead to the development of impaired interpersonal relationships and profound social disorders. However, the underlying cellular and molecular mechanisms involved are largely unknown. Here, we found that isolation of neonatal rats induced glucocorticoid-dependent social dominance over nonisolated control rats in juveniles from the same litter. Furthermore, neonatal isolation inactivated the actin-depolymerizing factor (ADF)/cofilin in the juvenile medial prefrontal cortex (mPFC). Isolation-induced inactivation of ADF/cofilin increased stable actin fractions at dendritic spines in the juvenile mPFC, decreasing glutamate synaptic AMPA receptors. Expression of constitutively active ADF/cofilin in the mPFC rescued the effect of isolation on social dominance. Thus, neonatal isolation affects spines in the mPFC by reducing actin dynamics, leading to altered social behavior later in life.


2010 ◽  
Vol 11 (1) ◽  
Author(s):  
Willard M Freeman ◽  
Melinda E Lull ◽  
Kruti M Patel ◽  
Robert M Brucklacher ◽  
Drake Morgan ◽  
...  

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