Publications by authors named "C Anacker"

Background: Perinatal depression is common: on average, more than 13% of women suffer from physician-diagnosed disorder and 20% report symptoms bearing clinical relevance. Maternal depression not only significantly impacts women's quality of life but also increases the offspring's risk of negative developmental outcomes, including mental disorders, through a combination of maternal alterations in biology and postnatal rearing factors during the early period of life. The HappyMums project aims to improve our understanding of perinatal depression by identifying the factors that robustly predict risk and resilience in mothers and their offspring, determining underlying neurobiological mechanisms, and, finally, testing the efficacy of potential interventions.

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Article Synopsis
  • Early Life Adversity (ELA) can lead to increased stress sensitivity in adulthood, particularly affecting females, but the neurobiological mechanisms behind this are not well understood.
  • In a study using mice, ELA was shown to decrease serotonin neuron activity and increase stress-related behaviors and hormone levels, while also reducing neurogenesis and increasing inflammation in specific brain regions.
  • Targeting serotonin 1A autoreceptors during development appears to prevent the negative impacts of ELA on stress responses and brain function in adult female mice, suggesting potential avenues for intervention.
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Early Life Adversity (ELA) predisposes to stress hypersensitivity in adulthood, but neurobiological mechanisms that protect from the enduring effects of ELA are poorly understood. Serotonin 1A (5HT ) autoreceptors in the raphé nuclei regulate adult stress vulnerability, but whether 5HT could be targeted to prevent ELA effects on susceptibility to future stressors is unknown. Here, we exposed mice with postnatal knockdown of 5HT autoreceptors to the limited bedding and nesting model of ELA from postnatal day (P)3-10 and tested behavioral, neuroendocrine, neurogenic, and neuroinflammatory responses to an acute swim stress in male and female mice in adolescence (P35) and in adulthood (P56).

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Objective: Metabolic Syndrome, which can be induced or exacerbated by current antipsychotic drugs (APDs), is highly prevalent in schizophrenia patients. Recent preclinical and clinical evidence suggest that agonists at trace amine-associated receptor 1 (TAAR1) have potential as a new treatment option for schizophrenia. Intriguingly, preclinical tudies have also identified TAAR1 as a novel regulator of metabolic control.

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Background: Hyperactivity of granule cells in the ventral dentate gyrus (vDG) promotes vulnerability to chronic stress. However, which receptors in the vDG could be targeted to inhibit this hyperactivity and confer stress resilience is not known. The serotonin 1A receptor (5-HTR) is a G protein-coupled inhibitory receptor that has been implicated in stress adaptation, anxiety, depression, and antidepressant responses.

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