In classical fear conditioning, a neutral conditioned stimulus (CS) is paired with an aversive unconditioned stimulus (US), which leads to a fear memory. If the CS is repeatedly presented without the US after fear conditioning, the formation of an extinction memory occurs, which inhibits fear memory expression. A previous study has demonstrated that selective cholinergic lesions in the medial septum and vertical limb of the diagonal bands of Broca (MS/vDBB) prior to fear and extinction learning disrupt contextual fear memory discrimination and acquisition of extinction memory. MS/vDBB cholinergic neurons project to a number of substrates that are critical for fear and extinction memory. However, it is currently unknown which of these efferent projections are critical for contextual fear memory discrimination and extinction memory. To address this, we induced cholinergic lesions in efferent targets of MS/vDBB cholinergic neurons. These included the dorsal hippocampus (dHipp), ventral hippocampus (vHipp), medial prefrontal cortex (mPFC), and in the mPFC and dHipp combined. None of these lesion groups exhibited deficits in contextual fear memory discrimination or extinction memory. However, vHipp cholinergic lesions disrupted auditory fear memory. Because MS/vDBB cholinergic neurons are the sole source of acetylcholine in the vHipp, these results suggest that MS/vDBB cholinergic input to the vHipp is critical for auditory fear memory. Taken together with previous findings, the results of this study suggest that MS/vDBB cholinergic neurons are critical for fear and extinction memory, though further research is needed to elucidate the role of MS/vDBB cholinergic neurons in these types of emotional memory.

Clinical and preclinical studies that have examined the neurobiology of persistent fear memory in posttraumatic stress disorder (PTSD) have focused on the medial prefrontal cortex, hippocampus, and amygdala. Sensory systems, the periaqueductal gray (PAG), and midline thalamic nuclei have been implicated in fear and extinction memory, but whether neural activity in these substrates is sensitive to traumatic stress (at baseline or during emotional learning and memory) remains unexplored. To address this, we used the single prolonged stress (SPS) model of traumatic stress. SPS and control rats were either subjected to fear conditioning (CS-fear) or presented with CSs alone (CS-only) during fear conditioning. All rats were then subjected to extinction training and testing. A subset of rats were euthanized after each behavioral stage and c-Fos and c-Jun used to measure neural activation in all substrates. SPS lowered c-Jun levels in the dorsomedial and lateral PAG at baseline, but the elevated c-Jun expression in the PAG during emotional learning and memory. SPS also altered c-Fos expression during fear and extinction learning/memory in midline thalamic nuclei. These findings suggest changes in neural function in the PAG and midline thalamic nuclei could contribute to persistent fear memory induced by traumatic stress. Interestingly, SPS effects were also observed in animals that never learned fear or extinction (i.e., CS-only). This raises the possibility that traumatic stress could have broader effects on the psychological function that are dependent on the PAG and midline thalamic nuclei.

Purpose: The purpose of this study was to assess the association between various risk factors with postpartum depression severity using a large dataset that included variables such as previous mental health status, social factors, societal factors, health care access, and other state-wide or region-specific variables.Methods: We obtained the most recently available (2016–2017) dataset from the Pregnancy Risk Assessment Monitoring System (PRAMS), which is a dataset compiled by the Centers for Disease Control (CDC) that collects state-specific, population-based data on maternal attitudes and experiences before, during, and shortly after pregnancy from over 73,000 women in 39 states. We utilized a hierarchical linear model to analyze the data across various levels, with a symptom severity scale (0–8) as the dependent variable.Results: Of the 21 variables included in the final model, nine variables were statistically significant predictors of symptom severity. Statistically significant predictors of increased postpartum depression symptom severity included previous depression diagnosis and depression symptoms during pregnancy, baby not residing with mother, unintentional pregnancy, women with less than a high school degree and more than a college degree, Women Infants Children (WIC) enrollment, and married women. In contrast to these other factors, attendance at a postpartum follow up appointment was associated with significantly increased symptom severity. Age revealed an inverted curve in predicting postpartum symptom severity.Conclusions: There was no significant difference in symptom severity scores across the 39 participating states. Most notably, postpartum depression symptom severity was associated with previous depression diagnosis and previous symptom severity, but our results also reveal novel social and education factors that contribute to the support and well-being of the mother and child.

Background A core symptom of post traumatic stress disorder (PTSD) is persistent fear memory, which can be defined as fear memory that is resistant to updating, inhibition, or extinction. PTSD emerges after traumatic stress exposure, but neurobiological mechanisms via which traumatic stress leads to persistent fear memory are not well defined. Akt signaling within the amygdala (Amy) is enhanced with traumatic stress and phosphatidylinositol kinase 3 (PI3K) activation of Akt within the basolateral amygdala (BLA) has been implicated as critical to fear memory formation. These findings raise the possibility that traumatic stress enhances PI3K → Akt signaling in the BLA, which leads to persistent fear memory. Methods To test this hypothesis rats were exposed to traumatic stress, using the single prolonged stress model, and changes in Akt phosphorylation (pAkt) were assayed in the Amy at 0 and 30 min after fear conditioning (FC). In a separate experiment we inhibited PI3K → Akt signaling in the BLA prior to FC and observed the effect this had on acquisition, expression, and extinction of FC in stressed and control rats. Results Enhanced pAkt in the Amy at both time points was observed in stressed rats, but not in control rats. PI3K → Akt inhibition in the BLA had no effect on freezing in control rats, but decreased freezing during extinction training and testing in stressed rats. Conclusion These findings suggest that PI3K → Akt signaling in the BLA could be a mechanism via which traumatic stress leads to fear memory that is resistant to extinction.

This study examined the effect of limited bedding and nesting (LBN) stress on postpartum anhedonia, maternal behaviors, anxiety‐like behaviors, and neuroendocrine and neuroimmune function as a potential model of postpartum depression. Dams underwent sucrose preference tests prior to breeding, during gestation and again postpartum, to examine the potential onset of anhedonia. On embryonic day 19, dams were placed into either a LBN or control housing condition. Contrary to our predictions, LBN stress had no effect on postpartum sucrose preference. We also found no effect of LBN condition on fecal estradiol or corticosterone levels, both of which increased at birth and decreased postpartum. Regardless of housing conditions, approximately 40% of new mothers exhibited a decrease in sucrose preference, while others show no change, suggesting an individual susceptibility to postpartum anhedonia. In a separate cohort of LBN and control dams, we measured pup retrieval, hoarding behavior, elevated plus maze (EPM), and marble burying. LBN dams exhibited increased anxiety, associated with decreased time spent in the open arms of the EPM. We also measured a significant increase in IL‐6 expression in the dorsal hippocampus and medial prefrontal cortex of postpartum dams compared to nonpregnant dams. These findings suggest that while LBN stress has effects on anxiety and maternal care, it does not induce postpartum anhedonia. Rather, there are inherent differences in susceptibility to anhedonia in individual dams, and future studies should be conducted to better understand individual vulnerability and resilience to postpartum anhedonia.

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