Approximately 15% of women who give birth develop postpartum depression (PPD), and the risk is greater in women who do not breastfeed or who cease breastfeeding early. In some women, early cessation or absence of breastfeeding precedes PPD, but the neuroendocrine mechanisms of this relationship are unknown. We tested whether nursing demand would alter behavioral and endocrine endpoints relevant for depression in postpartum rats. Adult female Sprague-Dawley rats underwent thelectomy (thel; removal of teats), sham surgery (sham), or no surgery (control). Litters were rotated between thel and sham rats every 12 h, yielding a higher nursing burden for sham rats. We investigated behavior in the forced swim test (FST), open field test, and sucrose preference test, and serum corticosterone (CORT) concentrations. Because the hippocampus changes structurally in depression and with maternal experience, we investigated cell proliferation using Ki-67 and hippocampal neurogenesis and immature neuron development using doublecortin (DCX) immunohistochemistry. Sham rats spent less time immobile in the FST compared with control and thel rats. Sham rats also had higher CORT concentrations and fewer Ki-67 cells. Thel rats had more DCX-expressing cells and a greater proportion of mature DCX-expressing cells compared with control and sham rats. These data suggest that greater nursing demand reduces stress-related behavioral responses despite increasing CORT concentrations and suppressing hippocampal neurogenesis. This work is an important step in identifying how lactation buffers behavioral responses to stress and reorganizes stress-related neural circuitry and is crucial for identifying mechanisms of postpartum psychiatric illnesses.
Keywords: Doublecortin; Ki-67; Lactation; Postpartum depression; Suckling stimulation.
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