[article]
| Titre : |
MeCP2 haplodeficiency and early-life stress interaction on anxiety-like behavior in adolescent female mice |
| Type de document : |
texte imprimé |
| Auteurs : |
María ABELLÁN-ÁLVARO, Auteur ; Oliver STORK, Auteur ; Carmen AGUSTÍN-PAVÓN, Auteur ; Mónica SANTOS, Auteur |
| Langues : |
Anglais (eng) |
| Mots-clés : |
Adverse Childhood Experiences Animals Anxiety/etiology Female Humans Hypothalamo-Hypophyseal System/metabolism Maternal Deprivation Methyl-CpG-Binding Protein 2/genetics/metabolism Mice Pituitary-Adrenal System/metabolism Arginine-vasopressin Corticotropin-releasing hormone Maternal separation Rett syndrome c-FOS |
| Index. décimale : |
PER Périodiques |
| Résumé : |
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. |
| En ligne : |
https://dx.doi.org/10.1186/s11689-021-09409-7 |
| Permalink : |
https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=574 |
in Journal of Neurodevelopmental Disorders > 13 (2021)
[article] MeCP2 haplodeficiency and early-life stress interaction on anxiety-like behavior in adolescent female mice [texte imprimé] / María ABELLÁN-ÁLVARO, Auteur ; Oliver STORK, Auteur ; Carmen AGUSTÍN-PAVÓN, Auteur ; Mónica SANTOS, Auteur. Langues : Anglais ( eng) in Journal of Neurodevelopmental Disorders > 13 (2021)
| Mots-clés : |
Adverse Childhood Experiences Animals Anxiety/etiology Female Humans Hypothalamo-Hypophyseal System/metabolism Maternal Deprivation Methyl-CpG-Binding Protein 2/genetics/metabolism Mice Pituitary-Adrenal System/metabolism Arginine-vasopressin Corticotropin-releasing hormone Maternal separation Rett syndrome c-FOS |
| Index. décimale : |
PER Périodiques |
| Résumé : |
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. |
| En ligne : |
https://dx.doi.org/10.1186/s11689-021-09409-7 |
| Permalink : |
https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=574 |
|  |
MeCP2 haplodeficiency and early-life stress interaction on anxiety-like behavior in adolescent female mice in Journal of Neurodevelopmental Disorders, 13 (2021)
