Blockade of corticotropin-releasing hormone receptor 1 attenuates early-life stress-induced synaptic abnormalities in the neonatal hippocampus

Hippocampus ◽  
2014 ◽  
Vol 24 (5) ◽  
pp. 528-540 ◽  
Author(s):  
Xue-Mei Liao ◽  
Xiao-Dun Yang ◽  
Jiao Jia ◽  
Ji-Tao Li ◽  
Xiao-Meng Xie ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone

Early-life stress-induced anxiety-related behavior in adult mice partially requires forebrain corticotropin-releasing hormone receptor 1

2012 ◽  
Vol 36 (3) ◽  
pp. 2360-2367 ◽  
Author(s):  
Xiao-Dong Wang ◽  
Christiana Labermaier ◽  
Florian Holsboer ◽  
Wolfgang Wurst ◽  
Jan M. Deussing ◽  
...  
Keyword(s):  
Hormone Receptor ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
Adult Mice

scholarly journals MeCP2 haplodeficiency and early-life stress interaction on anxiety-like behavior in adolescent female mice

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
María Abellán-Álvaro ◽  
Oliver Stork ◽  
Carmen Agustín-Pavón ◽  
Mónica Santos
Keyword(s):  
Life Stress ◽  
Early Life ◽  
Maternal Separation ◽  
Early Life Stress ◽  
Hypothalamic Nucleus ◽  
Corticotropin Releasing Hormone ◽  
Wild Type ◽  
Releasing Hormone ◽  
Complex Disorders ◽  
Female Mice

Abstract Background Early-life stress can leave persistent epigenetic marks that may modulate vulnerability to psychiatric conditions later in life, including anxiety, depression and stress-related disorders. These are complex disorders with both environmental and genetic influences contributing to their etiology. Methyl-CpG Binding Protein 2 (MeCP2) has been attributed a key role in the control of neuronal activity-dependent gene expression and is a master regulator of experience-dependent epigenetic programming. Moreover, mutations in the MECP2 gene are the primary cause of Rett syndrome and, to a lesser extent, of a range of other major neurodevelopmental disorders. Here, we aim to study the interaction of MeCP2 with early-life stress in variables known to be affected by this environmental manipulation, namely anxiety-like behavior and activity of the underlying neural circuits. Methods Using Mecp2 heterozygous and wild-type female mice we investigated the effects of the interaction of Mecp2 haplodeficiency with maternal separation later in life, by assessing anxiety-related behaviors and measuring concomitant c-FOS expression in stress- and anxiety-related brain regions of adolescent females. Moreover, arginine vasopressin and corticotropin-releasing hormone neurons of the paraventricular hypothalamic nucleus were analyzed for neuronal activation. Results In wild-type mice, maternal separation caused a reduction in anxiety-like behavior and in the activation of the hypothalamic paraventricular nucleus, specifically in corticotropin-releasing hormone-positive cells, after the elevated plus maze. This effect of maternal separation was not observed in Mecp2 heterozygous females that per se show decreased anxiety-like behavior and concomitant decreased paraventricular nuclei activation. Conclusions Our data supports that MeCP2 is an essential component of HPA axis reprogramming and underlies the differential response to anxiogenic situations later in life.

Sign in / Sign up

Export Citation Format

Share Document