Paternal Care Impacts Oxytocin Expression in California Mouse Offspring and Basal Testosterone in Female, but Not Male Pups

Natural variations in parenting are associated with differences in expression of several hormones and neuropeptides which may mediate lasting effects on offspring development, like regulation of stress reactivity and social behavior. Using the bi-parental California mouse, we have demonstrated that parenting and aggression are programmed, at least in part, by paternal behavior as adult offspring model the degree of parental behavior received in development and are more territorial following high as compared to low levels of care. Development of these behaviors may be driven by transient increases in testosterone following paternal retrievals and increased adult arginine vasopressin (AVP) immunoreactivity within the bed nucleus of the stria terminalis (BNST) among high-care (HC) offspring. It remains unclear, however, whether other neuropeptides, such as oxytocin (OT), which is sensitive to gonadal steroids, are similarly impacted by father-offspring interactions. To test this question, we manipulated paternal care (high and low care) and examined differences in adult offspring OT-immunoreactive (OT-ir) within social brain areas as well as basal T and corticosterone (Cort) levels. HC offspring had more OT-ir within the paraventricular nucleus (PVN) and supraoptic nucleus (SON) than low-care (LC) offspring. Additionally, T levels were higher among HC than LC females, but no differences were found in males. There were no differences in Cort indicating that our brief father-pup separations likely had no consequences on stress reactivity. Together with our previous work, our data suggest that social behavior may be programmed by paternal care through lasting influences on the neuroendocrine system

The role of 5-HT receptors in depression

Abstract Depression is a polygenic and highly complex psychiatric disorder that remains a major burden on society. Antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), are some of the most commonly prescribed drugs worldwide. In this review, we will discuss the evidence that links serotonin and serotonin receptors to the etiology of depression and the mechanisms underlying response to antidepressant treatment. We will then revisit the role of serotonin in three distinct hypotheses that have been proposed over the last several decades to explain the pathophysiology of depression: the monoamine, neurotrophic, and neurogenic hypotheses. Finally, we will discuss how recent studies into serotonin receptors have implicated specific neural circuitry in mediating the antidepressant response, with a focus being placed on the hippocampus