Lactation is not required for maintaining maternal care and active coping responses in chronically stressed postpartum rats: Interactions between nursing demand and chronic variable stress

Urocortin-3 neurons in the perifornical area mediate the impact of chronic stress on female infant-directed behavior

“…In mothers, chronic stress led to a decrease in PeFA Ucn3 /Fos levels compared to control lactating females, opposite to the effect we observed in virgin females (Figure 5G, H). Like virgin females, however, PVH CRF cell activation was significantly decreased in chronically stressed lactating females (Figure 5G, I; Supplemental Figure 5-1), consistent with previous literature (Girotti et al ., 2006; Radley & Sawchenko, 2015; Matovic et al ., 2020). We observed a similar negative trend for correlation of PeFA Ucn3 neuronal activation and parental behaviors in control lactating females that we observed in virgin females, but the trend for PVH CRF cell activation is positively correlated in lactating females (Figure 5 K, L).…”

“…The decrease in CORT and CRF neuronal activation are indicative of HPA axis habituation to the repeated stress. Indeed, previous studies have illustrated a reduction in CRF/Fos colabeling or electrophysiological properties of CRF neurons in the PVH with repeated restraint stress in rodents (Bonaz & Rivest, 1998; Matovic et al ., 2020). We interpret the decrease in Ucn3 neuronal activity as a protective mechanism, preserving maternal behavior under stressful conditions.…”

“…During lactation, females are hyporesponsive to acute stress due to hormonal changes that impact the Hypothalamic-Pituitary-Adrenal (HPA) axis regulation (Walker et al, 2001;Brunton et al, 2008). HPA axis hypo-responsivity is thought to be protective of anxiety-related behavior and adult-pup interactions in lactating females (Miller et al, 2011;Medina et al, 2021). However, chronic stress has been documented to have a long-lasting impact on the regulation of the HPA axis, leading to reduced parenting, and how the underlying neurobiology is affected remains poorly understood (Carini et al, 2013;Murgatroyd et al, 2015).…”

Mitochondrial might: powering the peripartum for risk and resilience

“…Preclinical studies in female rodents support a role for peripartum stress in the development of neuropsychiatric disorders such as PPD (summarized in Table 1). Exposure to stress before (Gemmel et al, 2018;Czarzasta et al, 2019) or, during gestation (Pardon et al, 2000;Smith et al, 2004;Misdrahi et al, 2005;O'Mahoney et al, 2006;Haim et al, 2014;Leuner et al, 2014;Gemmel et al, 2016;Gifford et al, 2023;Gorman-Sandler et al, 2023) or, in the postpartum period during lactation (Nephew and Bridges, 2011;Medina et al, 2021;Cruz et al, 2023) in the postpartum period during lactation, increases the expression of PPD-relevant behaviors including anhedonia and disrupted maternal care. Similarly, treating female rats with the steroid stress hormone, corticosterone, is sufficient to elicit anhedonia and decreased maternal care (Brummelte et al, 2006;Pawluski et al, 2009;Brummelte and Galea, 2010;Workman et al, 2013Workman et al, , 2016.…”