Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
It is becoming clear that the female brain has an inherent plasticity that is expressed during reproduction. The changes that occur benefit the offspring, which in turn secures the survival of the mother’s genetic legacy. Thus, the onset of maternal motivation involves basic mechanisms from genetic expression profiles, to hormone release, to hormone-neuron interactions, all of which fundamentally change the neural architecture – and for a period of time that extends, interestingly, beyond the reproductive life of the female. Although multiple brain areas involved in maternal responses are discussed, this review focuses primarily on plasticity in the maternal hippocampus during pregnancy, the postpartum period and well into aging as it pertains to changes in cognition. In addition, the effects of prolonged and repeated stress on these dynamic responses are considered. The maternal brain is a marvel of directed change, extending into behaviors both obvious (infant-directed) and less obvious (predation, cognition). In sum, the far-reaching effects of reproduction on the female nervous system provide an opportunity to investigate neuroplasticity and behavioral flexibility in a natural mammalian model.
ISSN: 0018-506X

hal-01169791
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01169791
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01169791/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01169791/file/Neuroplasticity%20In%20The%20Maternal%20Hippocampus_accepted.pdf
DOI : 10.1016/j.yhbeh.2015.06.004

Éditeur(s) : HAL CCSD Wiley
Résumé : International audience
With the growing use of selective serotonin reuptake inhibitor medications (SSRIs) for the treatment of depression during the perinatal period, questions have been raised about the longterm impact of these medications on development. We aimed to investigate how developmental SSRI exposure may alter affect-related behaviors and associated molecular processes in offspring using a rodent model of maternal stress and depression. For this purpose, prenatally stressed or non-stressed male offspring were exposed to fluoxetine (5 mg/kg/day) or vehicle, via lactation, until weaning. Primary results show that postnatal fluoxetine exposure differentially altered anxiety-like behavior by increasing anxiety in non-stressed offspring and decreasing anxiety in prenatally stressed offspring. In the hippocampus, developmental fluoxetine exposure decreased BDNF IV and TrkB mRNA expression. Prenatal stress alone also decreased escape behaviors and decreased hippocampal BDNF IV mRNA expression. These data provide important evidence for the long-term programming effects of early-life exposure to SSRIs on brain and behavior.
ISSN: 0012-1630

hal-01305478
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01305478
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01305478/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01305478/file/Developmental%20SSRIs%2C%20anxiety%20and%20BDNF_accepted.pdf
DOI : 10.1002/dev.21385

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
o abstract
ISSN: 0306-4530

hal-01390972
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01390972
DOI : 10.1016/j.psyneuen.2016.07.096

Éditeur(s) : HAL CCSD Wiley
Résumé : International audience
Selective serotonin reuptake inhibitor medication exposure during the perinatal period can have a long term impact in adult offspring on neuroplasticity and the serotonergic system, but the impact of these medications during early development is poorly understood. The aim of this study was to determine the effects of developmental exposure to the SSRI, fluoxetine, on the serotonergic system, dopaminergic system, and synaptophysin density in the prefrontal cortex and hippocampus, as well as number of immature neurons in the dentate gyrus, in juvenile rat offspring at weaning. To model aspects of maternal depression, prenatal restraint stress was used. Sprague-Dawley rat offspring were exposed to either prenatal stress and/or fluoxetine. Main findings show that developmental fluoxetine exposure to prenatally stressed offspring decreased 5-HT and 5-HIAA levels and altered the dopaminergic system in the hippocampus. Prenatal stress, regardless of fluoxetine, increased synaptophysin density in the PFC. This work indicates that early exposure to maternal stress and SSRI medication can alter brain monoamine levels and synaptophysin density in offspring at weaning. © 2015 Wiley Periodicals, Inc. Dev Psychobiol
ISSN: 0012-1630

hal-01237091
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01237091
DOI : 10.1002/dev.21372
PUBMED : 26477449

Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
Ten to twenty percent of postpartum women experience anxiety or depressive disorders, which can have detrimental effects on the mother, child, and family. Little is known about the neural correlates of these affective disorders when they occur in mothers, but they do have unique neural profiles during the postpartum period compared with when they occur at other times in a woman's life. Given that the neural systems affected by postpartum anxiety and depression overlap and interact with the systems involved in maternal caregiving behaviors, mother–infant interactions are highly susceptible to disruption. Thus, there is an intricate interplay among maternal mental health, the mother–infant relationship, and the neurobiological mechanisms mediating them that needs to be the focus of future study.
ISSN: 0166-2236

hal-01452985
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01452985
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01452985/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01452985/file/The%20Neurobiology%20of%20Postpartum-Tins%20Manscript%20REVISED%20clean%201.pdf
DOI : 10.1016/j.tins.2016.11.009

Éditeur(s) : HAL CCSD
Résumé : International audience
Selective serotonin reuptake inhibitor medications (SSRIs) are the first lines of treatment for maternal affective disorders, and are prescribed to up to 10% of pregnant women. Concern has been raised about how perinatal exposure to these medications affect offspring neurobehavioral outcomes, particularly those related to social interactions, as recent research has reported conflicting results related to autism spectrum disorder (ASD) risk in children prenatally exposed to SSRIs. Therefore, the aim of this work was to investigate the effects of perinatal exposure to the SSRI fluoxetine on social play behaviors and the hypothalamic pituitary adrenal system, using a model of pre-gestational maternal stress. We also investigated synaptic proteins in the CA2, CA3, and dentate gyrus of the hippocampus, as well as number of immature neurons in the granule cell layer, as both measures of plasticity in the hippocampus have been linked to social behaviors. In pre-adolescent male and female Sprague-Dawley rat offspring, main findings show that perinatal fluoxetine prevents the negative effect of maternal stress on sibling play behavior. However, perinatal fluoxetine increased social aggressive play with a novel conspecific in both sexes and decreased time grooming a novel conspecific in males only. Perinatal fluoxetine also increased serum corticosteroid binding globulin levels, 5-HT levels in the hippocampus, and pre-synaptic density assessed via synaptophysin in the dentate gyrus. Social interaction was significantly correlated with changes in plasticity in the CA2 region of the hippocampus. Pre-gestational maternal stress exposure resulted in significantly decreased rates of hippocampal neurogenesis and synaptophysin density in the dentate gyrus of pre-adolescent males, but not females. Together, these results further characterize the role of perinatal SSRIs, maternal stress prior to conception, and sex/gender on developing social behaviors and related plasticity in the hippocampus of pre-adolescent offspring.
Psychoneuroendocrinology

hal-01579611
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01579611
DOI : 10.1016/j.psyneuen.2017.07.480
PUBMED : 28735226

Éditeur(s) : HAL CCSD Elsevier - International Brain Research Organization
Résumé : International audience
Women are more likely to develop depression during childbearing years with up to 20% of women suffering from depression during pregnancy and in the postpartum period. Increased prevalence of depression during the perinatal period has resulted in frequent selective serotonin reuptake inhibitor (SSRI) antidepressant treatment; however the effects of such medications on the maternal brain remain limited. Therefore, the aim of the present study is to investigate the effects of the SSRI medication, fluoxetine, on neurobiological differences in the maternal brain. To model aspects of maternal depression, gestational stress was used. Sprague-Dawley rat dams were exposed to either gestational stress and/or fluoxetine (5mg/kg/day) to form the following four groups: 1. Control+Vehicle, 2. Stress+Vehicle, 3. Control+Fluoxetine 4. Stress+Fluoxetine. At weaning maternal brains were collected. Main findings show that gestational stress alone increased synaptophysin and serotonin metabolism in the CG2 region of the cortex while fluoxetine treatment after stress normalized these effects. In the hippocampus, fluoxetine treatment, regardless of gestational stress exposure, decreased both global measures of methylation in the dentate gyrus, as measured by Dnmt3a immunoreactivity, as well as serotonin metabolism. No further changes in synaptophysin, PSD-95, or Dnmt3a immunoreactivity were seen in the cortical or hippocampal areas investigated. These findings show that gestational stress and SSRI medication affect the neurobiology of the maternal brain in a region-specific manner. This work adds to a much needed area of research aimed at understanding neurobiological changes associated with maternal depression and the role of SSRI treatment in altering these changes in the female brain
ISSN: 0306-4522

hal-01301509
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01301509
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01301509/document
https://hal-univ-rennes1.archives-ouvertes.fr/hal-01301509/file/Gestational%20stress%20and%20fluoxetine%20treatment%20%281%29.pdf
PUBMED : 27060483