scholarly journals Memories of an Autopsy: The Effects of Stress Exposure on Suggestibility for a Stressful Event

2013 ◽  
Vol 5 (1) ◽  
Author(s):  
Elisa Krackow ◽  
Vanessa M. Jacoby ◽  
Joseph R. Scotti
2018 ◽  
Author(s):  
Mohammed Mostafizur Rahman ◽  
Ashutosh Shukla ◽  
Sumantra Chattarji

AbstractStress is known to exert its detrimental effects not only by enhancing fear, but also by impairing its extinction. However, in earlier studies stress exposure invariably preceded both processes. Thus, compared to unstressed animals, stressed animals had to extinguish fear memories from higher levels of freezing caused by prior exposure to stress. Here we decouple the two processes to examine if stress specifically impairs fear extinction. Strikingly, when fear memories were formed before stress exposure, thereby allowing animals to initiate extinction from comparable levels of fear, recall of fear extinction was unaffected. Despite this we observed a persistent increase in theta activity in the BLA. Theta activity in the mPFC, by contrast, was normal. Stress also disrupted mPFC-BLA theta-frequency synchrony and directional coupling. Thus, in the absence of the fear-enhancing effects of stress, the expression of fear reflects normal regulation of mPFC activity, not stress-induced hyperactivity in the amygdala.


2021 ◽  
Vol 12 ◽  
Author(s):  
Caroline Baynard ◽  
Thomas E. Prisinzano ◽  
Eduardo R. Butelman

The kappa-opioid receptor (KOR) / dynorphin system is implicated with behavioral and neurobiological effects of stress exposure (including heavy exposure to drugs of abuse) in translational animal models. Thus some KOR-antagonists can decrease the aversive, depressant-like and anxiety-like effects caused by stress exposure. The first generation of selective KOR-antagonists have slow onsets (hours) and extremely long durations of action (days-weeks), in vivo. A new generation of KOR antagonists with rapid onset and shorter duration of action can potentially decrease the effects of stress exposure in translational models, and may be of interest for medication development. This study examined the rapid onset anti-stress effects of one of the shorter acting novel KOR-antagonists (LY2795050, (3-chloro-4-(4-(((2S)-2-pyridin-3-ylpyrrolidin-1-yl)methyl) phenoxy)benzamide)) in a single-session open space swim (OSS) stress paradigm (15 min duration), in adult male and female C57BL/6 J mice. LY2795050 (0.32 mg/kg, i.p.) had rapid onset (within 15 min) and short duration (<3 h) of KOR-antagonist effects, based on its blockade of the locomotor depressant effects of the KOR-agonist U50,488 (10 mg/kg). LY2795050 (0.32 mg/kg), when administered only 1 min prior to the OSS stress paradigm, decreased immobility in males, but not females. With a slightly longer pretreatment time (15 min), this dose of LY2795050 decreased immobility in both males and females. A 10-fold smaller dose of LY2795050 (0.032 mg/kg) was inactive in the OSS, showing dose-dependence of this anti-stress effect. Overall, these studies show that a novel KOR-antagonist can produce very rapid onset anti-immobility effects in this model of acute stress exposure.


PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245444
Author(s):  
Megan Arnot ◽  
Emily H. Emmott ◽  
Ruth Mace

Many women going through the menopausal transition experience vasomotor symptoms (VMS), and research has shown that there is a large amount of variation in their frequency and severity. Many lifestyle factors have been found to co-vary with VMS, including the level of social support received by the woman, and how stressed she is. Stress is well documented to worsen menopause symptoms, and there is some evidence that support eases them; however, there is little research into whether support is an effective buffer against the negative effects of stress on VMS. Using nine years of data from the Study of Women’s Health Across the Nation (n = 2718), we use multilevel Poisson regression with random effects to test: 1) if more social support is associated with decreased VMS frequency, 2) if increased life stress worsens VMS, and 3) if support acts as a buffer against stress. After adjusting for age, marital status, smoking, self-perceived overall health, ethnicity, and menopausal status, we find that stress increases the frequency of VMS. Contrary to our hypothesis, we did not find strong evidence that emotional support led to lower VMS frequency, or that support buffers against the effects of stress. Experience of a stressful event, but not amount of social support, was included in the best fitting model; with the degree to which the woman was upset by the life stressor having the largest effect on menopause symptoms. Here, women who said they were currently upset by a stressful event experienced 21% more VMS than women who had experienced no life stressor. This research highlights that social factors may impact the menopausal transition.


eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Mohammed Mostafizur Rahman ◽  
Ashutosh Shukla ◽  
Sumantra Chattarji

Stress is known to exert its detrimental effects not only by enhancing fear, but also by impairing its extinction. However, in earlier studies stress exposure preceded both processes. Thus, compared to unstressed animals, stressed animals had to extinguish fear memories that were strengthened by prior exposure to stress. Here, we dissociate the two processes to examine if stress specifically impairs the acquisition and recall of fear extinction. Strikingly, when fear memories were formed before stress exposure, thereby allowing animals to initiate extinction from comparable levels of fear, recall of fear extinction was unaffected. Despite this, we observed a persistent increase in theta activity in the BLA. Theta activity in the mPFC, by contrast, was normal. Stress also disrupted mPFC-BLA theta-frequency synchrony and directional coupling. Thus, in the absence of the fear-enhancing effects of stress, the expression of fear during and after extinction reflects normal regulation of theta activity in the mPFC, not theta hyperactivity in the amygdala.


2002 ◽  
Vol 4 (2) ◽  
pp. 139-147

It has become increasingly clear that males and females differ even more dramatically than we previously thought. Not only do they exhibit differing responses to stress and environmental experience, but they can also respond in opposite directions. In rats, it has been shown that exposure to an acute stressful event can enhance subsequent learning in males while dramatically impairing learning in females. These opposite effects of stress on memory formation are accompanied by similarly opposite effects on neuroanatomical measures, such as dendritic spines in the hippocampal formation. Moreover, these opposite effects of stress are mediated by different hormonal systems between the sexes. These unique responses to stressful experience in male versus female rats may be used to model sex differences in mental illness, such as those that exist for depression and posttraumatic stress disorder.


2020 ◽  
Author(s):  
Alireza Chenani ◽  
Ghabiba Weston ◽  
Alessandro F. Ulivi ◽  
Tim P. Castello-Waldow ◽  
Alon Chen ◽  
...  

ABSTRACTStress exposure strongly contributes to the pathophysiology of psychiatric diseases such as depression, schizophrenia, anxiety, and post-traumatic stress disorder. It also affects both function and structure of hippocampal CA1, leading to episodic memory impairment. Here, we used deep-brain optical imaging to elucidate the effects of stress on CA1 pyramidal neuron structural connectivity and activity.We tracked dynamics of dendritic spines during repeated stress and found decrease in spinogenesis followed by decrease in spine stability. In contrast to repeated stress, acute stress led to stabilization of the spines born in temporal proximity to the stressful event. To investigate the link between structural plasticity and activity patterns upon repeated stress, we studied the activity of thousands of CA1 pyramidal neurons in freely-moving. We found an increase in activity and loss of temporal organization followed by a disruption in temporal and spatial coding. Our data suggest that stress-induced sustained increase in activity leads to loss of structural connectivity and subsequent temporal and spatial coding impairments.


2007 ◽  
Vol 24 (2) ◽  
pp. 139-148 ◽  
Author(s):  
M.E. Guerzoni ◽  
P. Vernocchi ◽  
M. Ndagijimana ◽  
A. Gianotti ◽  
R. Lanciotti

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