This is the unspecified version of the paper.This version of the publication may differ from the final published version. Permanent repository link: AbstractThere is converging evidence that 1 to 2% of women develop post-traumatic stress disorder (PTSD) as a result of childbirth. The current study aimed to explore the long-term effects of childbirth-related PTSD on women, their relationship with their partner, and their relationship with their child. Semi-structured interviews were carried out with six women who reported clinically significant PTSD after birth, ranging from 7 months to 18 years beforehand. Interviews were transcribed and analysed using thematic analysis. Childbirth-related PTSD was found to have wide ranging effects on women and their relationships. Women reported changes in physical wellbeing, mood and behaviour, social interaction, and fear of childbirth. Women reported negative effects on their relationship with their partner including sexual dysfunction, disagreements, and blame for events of birth. The mother-baby bond was also seriously affected.Nearly all women reported initial feelings of rejection towards the baby but this changed over time. Long-term, women seemed to have either avoidant or anxious attachments with their child.It is concluded that childbirth-related PTSD can have severe and lasting effects on women and their relationships with their partner and children. Further research is needed to compare this to normal difficulties experienced by women after having children. To date, most research has concentrated on the prevalence and causes of postnatal PTSD.Diathesis-stress approaches to mental health emphasise that whether a woman develops chronic postnatal PTSD will be influenced to varying degrees by pre-existing vulnerability and beliefs, the events of birth, and postnatal factors such as additional stress, support, and the meaning attached to the events of birth and symptoms of PTSD (Ayers, 2004;Beck, 2004a). Research supports this approach and suggests postnatal PTSD is associated with a previous history of trauma, history of psychological problems, and events during birth such as type of delivery (Ayers, 2004;Olde, van der Hart, Kleber, & Van Son, 2006). 4The effects of postnatal PTSD on women and their relationships with their child and partner have not been widely examined but have been subject to speculation (Bailham & Joseph, 2003). Case studies and qualitative research suggest it is likely that postnatal PTSD will affect women's close relationships. For example, in qualitative studies of postnatal PTSD, women report that it affects their sense of self, that they have less patience, feelings of anger, anxiety, depression, find it hard to sympathise with others, feel isolated from their infant, fear future pregnancy, and that it affects social relationships (Allen, 1998;Beck, 2004a). However, these qualitative studies did not assess PTSD using diagnostic criteria. Case studies, in which women do fulfil diagnostic criteria, suggest postnatal PTSD is associated with sex...

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The hippocampus (HPC) is known to play an important role in learning, a process dependent on synaptic plasticity; however, the molecular mechanisms underlying this are poorly understood. ⌬FosB is a transcription factor that is induced throughout the brain by chronic exposure to drugs, stress, and variety of other stimuli and regulates synaptic plasticity and behavior in other brain regions, including the nucleus accumbens. We show here that ⌬FosB is also induced in HPC CA1 and DG subfields by spatial learning and novel environmental exposure. The goal of the current study was to examine the role of ⌬FosB in hippocampal-dependent learning and memory and the structural plasticity of HPC synapses. Using viral-mediated gene transfer to silence ⌬FosB transcriptional activity by expressing ⌬JunD (a negative modulator of ⌬FosB transcriptional function) or to overexpress ⌬FosB, we demonstrate that HPC ⌬FosB regulates learning and memory. Specifically, ⌬JunD expression in HPC impaired learning and memory on a battery of hippocampaldependent tasks in mice. Similarly, general ⌬FosB overexpression also impaired learning. ⌬JunD expression in HPC did not affect anxiety or natural reward, but ⌬FosB overexpression induced anxiogenic behaviors, suggesting that ⌬FosB may mediate attentional gating in addition to learning. Finally, we found that overexpression of ⌬FosB increases immature dendritic spines on CA1 pyramidal cells, whereas ⌬JunD reduced the number of immature and mature spine types, indicating that ⌬FosB may exert its behavioral effects through modulation of HPC synaptic function. Together, these results suggest collectively that ⌬FosB plays a significant role in HPC cellular morphology and HPC-dependent learning and memory.

Post-traumatic stress disorder (PTSD) is a common, costly, and often debilitating psychiatric condition. However, the biological mechanisms underlying this disease are still largely unknown or poorly understood. Considerable evidence indicates that PTSD results from dysfunction in highly-conserved brain systems involved in stress, anxiety, fear, and reward. Pre-clinical models of traumatic stress exposure are critical in defining the neurobiological mechanisms of PTSD, which will ultimately aid in the development of new treatments for PTSD. Single prolonged stress (SPS) is a pre-clinical model that displays behavioral, molecular, and physiological alterations that recapitulate many of the same alterations observed in PTSD, illustrating its validity and giving it utility as a model for investigating post-traumatic adaptations and pre-trauma risk and protective factors. In this manuscript, we review the present state of research using the SPS model, with the goals of (1) describing the utility of the SPS model as a tool for investigating post-trauma adaptations, (2) relating findings using the SPS model to findings in patients with PTSD, and (3) indicating research gaps and strategies to address them in order to improve our understanding of the pathophysiology of PTSD.

Major depressive disorder is thought to arise in part from dysfunction of the brain's “reward circuitry,” consisting of the mesolimbic dopamine system and the glutamatergic and neuromodulatory inputs onto this system. Both chronic stress and antidepressant treatment regulate gene transcription in many of the brain regions that make up these circuits, but the exact nature of the transcription factors and target genes involved in these processes remain unclear. Here, we demonstrate induction of the FosB family of transcription factors in ∼25 distinct regions of adult mouse brain, including many parts of the reward circuitry, by chronic exposure to the antidepressant fluoxetine. We further uncover specific patterns of FosB gene product expression (i.e., differential expression of full-length FosB, ΔFosB, and Δ2ΔFosB) in brain regions associated with depression – the nucleus accumbens (NAc), prefrontal cortex (PFC), and hippocampus – in response to chronic fluoxetine treatment, and contrast these patterns with differential induction of FosB isoforms in the chronic social defeat stress model of depression with and without fluoxetine treatment. We find that chronic fluoxetine, in contrast to stress, causes induction of the unstable full-length FosB isoform in the NAc, PFC, and hippocampus even 24 hours following the final injection, indicating that these brain regions may undergo chronic activation when fluoxetine is on board, even in the absence of stress. We also find that only the stable ΔFosB isoform correlates with behavioral responses to stress. These data suggest that NAc, PFC, and hippocampus may present useful targets for directed intervention in mood disorders (ie, brain stimulation or gene therapy), and that determining the gene targets of FosB-mediated transcription in these brain regions in response to fluoxetine may yield novel inroads for pharmaceutical intervention in depressive disorders.