scholarly journals Predator odor increases glutamatergic synaptic transmission in the prelimbic cortex via corticotropin-releasing factor receptor 1 signaling

2018 ◽  
Author(s):  
Lara S. Hwa ◽  
Melanie M. Pina ◽  
Sofia Neira ◽  
Dipanwita Pati ◽  
Rachel Calloway ◽  
...  
Keyword(s):  
Stress Responses ◽  
Corticotropin Releasing Factor ◽  
Predator Odor ◽  
Acute Exposure ◽  
Post Traumatic Stress ◽  
Excitatory Transmission ◽  
Glutamatergic Synaptic Transmission ◽  
Bath Application ◽  
Defensive Burying ◽  
Synaptic Drive

ABSTRACTAcute exposure to a salient stressor, such as in post-traumatic stress disorder, can have lasting impacts upon an individual and society. To study stress in rodents, some naturalistic methods have included acute exposure to a predator odor, such as the synthetized fox odor 2,4,5, trimethyl-3-thiazoline (TMT). These experiments explore the stress-related behaviors and cortical activity induced by TMT exposure in adult male C57BL/6J mice and the influence of the stress neuropeptide, corticotropin-releasing factor (CRF) on these responses. Compared to H2O, mice exposed to TMT in the home cage showed increased avoidance and defensive burying indicative of evident stress responses. Consistent with stress-induced activation of the medial prefrontal cortex (mPFC), we found that the prelimbic (PL) and infralimbic (IL) subregions of the mPFC had elevated c-Fos immunolabeling after TMT compared to H2O. Slice physiology recordings were performed in layers 2/3 and 5 of the PL and IL, following TMT or H2O exposure. In TMT mice, PL layers 2/3 showed heightened spontaneous excitatory post-synaptic currents and synaptic drive, suggesting TMT enhanced excitatory transmission. Synaptic drive in PL was increased in both TMT and H2O mice following bath application of CRF, and systemic pretreatment with the CRF-R1 antagonist CP154526 reduced excitatory transmission in TMT mice, but not H2O mice. CP154526 also reduced stress-reactive behaviors induced by TMT.

scholarly journals The Role of Central Amygdala Corticotropin-Releasing Factor in Predator Odor Stress-Induced Avoidance Behavior and Escalated Alcohol Drinking in Rats

2019 ◽  
Author(s):  
Marcus M. Weera ◽  
Allyson L. Schreiber ◽  
Elizabeth M. Avegno ◽  
Nicholas W. Gilpin
Keyword(s):  
Alcohol Drinking ◽  
Avoidance Behavior ◽  
Conditioned Avoidance ◽  
Corticotropin Releasing Factor ◽  
Predator Odor ◽  
Central Amygdala ◽  
Post Traumatic Stress ◽  
Conditioned Place Avoidance ◽  
Place Avoidance ◽  
Post Traumatic

ABSTRACTPost-traumatic stress disorder (PTSD) is characterized by avoidance of trauma-associated stimuli and amygdala hyperreactivity, and is highly co-morbid with alcohol use disorder (AUD). Our lab uses a predator odor (bobcat urine) stress model that produces conditioned avoidance of an odor-paired context in a subset of rats, mirroring avoidance symptoms that manifest in some but not all humans exposed to trauma. We previously showed that after predator odor stress, Avoiders exhibit escalated alcohol drinking, higher aversion-resistant operant alcohol responding, hyperalgesia, and greater anxiety-like behavior compared to unstressed Controls. We also showed that systemic antagonism of corticotropin-releasing factor-1 receptors (CRFR1) reduced escalation of alcohol drinking in rats not indexed for avoidance, that corticotropin-releasing factor (CRF) infusions into the central amygdala (CeA) produced conditioned place avoidance in stress-naïve rats, and that intra-CeA infusion of a CRFR1 antagonist reduced hyperalgesia in Avoiders. Here, we show that avoidance behavior is persistent after repeated predator odor exposure and is resistant to extinction. In addition, Avoiders showed lower weight gain than Controls after predator odor re-exposure. In the brain, higher avoidance was correlated with higher number of c-Fos+ cells and CRF immunoreactivity in the CeA. Finally, we show that intra-CeA CRFR1 antagonism reversed post-stress escalation of alcohol drinking and reduced avoidance behavior in Avoiders. Collectively, these findings suggest that elucidation of the mechanisms by which CRFR1-gated CeA circuits regulate avoidance behavior and alcohol drinking may lead to better understanding of the neural mechanisms underlying co-morbid PTSD and AUD.

Increased ACTH response to corticotropin-releasing factor in cold-adapted rats in vivo

1989 ◽  
Vol 257 (3) ◽  
pp. E336-E339 ◽  
Author(s):  
A. Uehara ◽  
Y. Habara ◽  
A. Kuroshima ◽  
C. Sekiya ◽  
Y. Takasugi ◽  
...  
Keyword(s):  
Stress Responses ◽  
Cold Adaptation ◽  
Corticotropin Releasing Factor ◽  
Plasma Acth ◽  
Cold Adapted ◽  
Repeated Restraint Stress ◽  
Cross Adaptation ◽  
Freely Moving ◽  
Increased Activity

We have recently reported that chronically repeated restraint stress results in improved cold tolerance in rats via an increased activity of nonshivering thermogenesis, a characteristic metabolic change observed during cold adaptation, suggesting the presence of cross-adaptation between cold and stress. It is well established that the hypothalamic-pituitary-adrenal (HPA) axis is activated in various stress responses. In the present study, therefore, we examined whether cold adaptation would alter the adrenocorticotropic hormone (ACTH)-releasing state in vivo using freely moving, conscious rats chronically implanted with intra-atrial cannulas. There was no difference in the basal levels of plasma ACTH between warm control and cold-adapted rats. On the other hand, the ACTH response to the intravenous administration of corticotropin-releasing factor (CRF; 2 micrograms/animal) was significantly elevated in cold-adapted rats. However, the injection of 10 micrograms of CRF, which was considered as a dose to elicit the maximal ACTH response, resulted in similar ACTH release patterns between the two groups. These changes in the responsiveness of ACTH secretion have been observed in rats chronically exposed to stressful conditions. The results demonstrated in the present study, therefore, provide further evidence for our hypothesis that there may exist cross-adaptation between cold and nonthermal stress.

Y5 Receptors Mediate Neuropeptide Y Actions at Excitatory Synapses in Area CA3 of the Mouse Hippocampus

2002 ◽  
Vol 87 (1) ◽  
pp. 558-566 ◽  
Author(s):  
Hui Guo ◽  
Peter A. Castro ◽  
Richard D. Palmiter ◽  
Scott C. Baraban
Keyword(s):  
Synaptic Transmission ◽  
Neuropeptide Y ◽  
Critical Role ◽  
Hippocampal Slices ◽  
Receptor Subtype ◽  
Limbic Seizures ◽  
Excitatory Transmission ◽  
Npy Receptor ◽  
Bath Application ◽  
Peptide Agonist

Neuropeptide Y (NPY) is a potent modulator of excitatory synaptic transmission and limbic seizures. NPY is abundantly expressed in the dentate gyrus and is thought to modulate hippocampal excitability via activation of presynaptic Y2 receptors (Y2R). Here we demonstrate that NPY, and commonly used Y2R-preferring (NPY13–36) and Y5 receptor (Y5R)–preferring ([d-Trp32]NPY and hPP) peptide agonists, evoke similar levels of inhibition at excitatory CA3 synapses in hippocampal slices from wild-type control mice (WT). In contrast, NPYergic inhibition of excitatory CA3 synaptic transmission is absent in mice lacking the Y5R subtype (Y5R KO). In both analyses of evoked population spike activity and spontaneous excitatory postsynaptic synaptic currents (EPSCs), NPY agonists induced powerful inhibitory effects in all hippocampal slices from WT mice, whereas these peptides had no effect in slices from Y5R KO mice. In slices from WT mice, NPY (and NPY receptor–preferring agonists) reduced the frequency of spontaneous EPSCs but had no effect on sEPSC amplitude, rise time, or decay time. Furthermore, NPYergic modulation of spontaneous EPSCs in WT mice was mimicked by bath application of a novel Y5R-selective peptide agonist ([cpp]hPP) but not the selective Y2R agonist ([ahx5–24]NPY). In situ hybridization was used to confirm the presence of NPY, Y2, and Y5 mRNA in the hippocampus of WT mice and the absence of Y5R in knockout mice. These results suggest that the Y5 receptor subtype, previously believed to mediate food intake, plays a critical role in modulation of hippocampal excitatory transmission at the hilar-to-CA3 synapse in the mouse.

scholarly journals Resilience: Safety in the Aftermath of Traumatic Stressor Experiences

2020 ◽  
Vol 14 ◽  
Author(s):  
Kimberly Matheson ◽  
Ajani Asokumar ◽  
Hymie Anisman
Keyword(s):  
Stress Responses ◽  
Historical Trauma ◽  
Well Being ◽  
Traumatic Experiences ◽  
Post Traumatic Stress ◽  
Safe Place ◽  
Coping Responses ◽  
Biological Stress ◽  
Adverse Experiences ◽  
The Individual

The relationship between adverse experiences and the emergence of pathology has often focused on characteristics of the stressor or of the individual (stressor appraisals, coping strategies). These features are thought to influence multiple biological processes that favor the development of mental and physical illnesses. Less often has attention focused on the aftermath of traumatic experiences, and the importance of safety and reassurance that is necessary for longer-term well-being. In some cases (e.g., post-traumatic stress disorder) this may be reflected by a failure of fear extinction, whereas in other instances (e.g., historical trauma), the uncertainty about the future might foster continued anxiety. In essence, the question becomes one of how individuals attain feelings of safety when it is fully understood that the world is not necessarily a safe place, uncertainties abound, and feelings of agency are often illusory. We consider how individuals acquire resilience in the aftermath of traumatic and chronic stressors. In this respect, we review characteristics of stressors that may trigger particular biological and behavioral coping responses, as well as factors that undermine their efficacy. To this end, we explore stressor dynamics and social processes that foster resilience in response to specific traumatic, chronic, and uncontrollable stressor contexts (intimate partner abuse; refugee migration; collective historical trauma). We point to resilience factors that may comprise neurobiological changes, such as those related to various stressor-provoked hormones, neurotrophins, inflammatory immune, microbial, and epigenetic processes. These behavioral and biological stress responses may influence, and be influenced by, feelings of safety that come about through relationships with others, spiritual and place-based connections.

Effects of Support Groups on Post Traumatic Stress Responses in Women Experiencing Stillbirth

2007 ◽  
Vol 55 (1) ◽  
pp. 71-90 ◽  
Author(s):  
Joanne Cacciatore
Keyword(s):  
Support Groups ◽  
Support Group ◽  
Stress Responses ◽  
Traumatic Stress ◽  
Post Traumatic Stress ◽  
Impact Of Event Scale ◽  
Event Scale ◽  
Quantitative Results ◽  
Post Traumatic ◽  
The Impact

This research study explores the effects of support groups on traumatic stress responses of women experiencing stillbirth. Women ( N = 47) responded to a mixed method questionnaire. Quantitative results utilizing the Impact of Event Scale Revised demonstrate that women who attend support group, when controlling for time, had fewer post traumatic stress symptoms than did the women who did not attend support group. Qualitative results elucidate the role of support groups in managing grief, suggesting that connectivity with other like women may be a useful strategy in reducing problematic psychological outcomes.

The Role of Glucocorticoids in the (Mal)adaptive Response to Traumatic Experience

2018 ◽  
Author(s):  
Hagit Cohen ◽  
Joseph Zohar
Keyword(s):  
Stress Responses ◽  
Biological Data ◽  
The Body ◽  
Traumatic Experience ◽  
Post Traumatic Stress ◽  
Memory Integration ◽  
Response To Stress ◽  
Post Traumatic ◽  
Basic Facts

Glucocorticoids (GCs) play a major role in orchestrating the complex physiological and behavioral reactions essential for the maintenance of homeostasis. These compounds enable the organism to prepare for, respond to, and cope with the acute demands of physical and emotional stressors and enable a faster recovery with passage of the threat. A timely and an appropriate GC release commensurate with stressor severity enables the body to properly contain stress responses so as to promote recovery by rapidly restoring homeostasis. Inadequate GC release following stress not only delays recovery by disrupting biological homeostasis but can also interfere with the processing or interpretation of stressful information that results in long-term disruptions in memory integration. A salient example of such an impaired post-traumatic process is post-traumatic stress disorder (PTSD). The findings from recent animal models and translational and clinical neuroendocrine studies summarized in this chapter provide insights shedding light on the apparently contradictory studies of the HPA-axis response to stress. Also included is a review of the basic facts about PTSD and biological data.

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