scholarly journals Electroconvulsive Shock Does Not Impair the Reconsolidation of Cued and Contextual Pavlovian Threat Memory

2020 ◽  
Vol 21 (19) ◽  
pp. 7072
Author(s):  
Hajira Elahi ◽  
Veronica Hong ◽  
Jonathan E. Ploski
Keyword(s):  
Electroconvulsive Shock ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Memory Retrieval ◽  
Memory Trace ◽  
Stress Disorder ◽  
Fear Memory ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Electroconvulsive Seizure

Existing memories, when retrieved under certain circumstances, can undergo modification through the protein synthesis-dependent process of reconsolidation. Disruption of this process can lead to the weakening of a memory trace, an approach which is being examined as a potential treatment for disorders characterized by pathological memories, such as Post-Traumatic Stress Disorder. The success of this approach relies upon the ability to robustly attenuate reconsolidation; however, the available literature brings into question the reliability of the various drugs used to achieve such a blockade. The identification of a drug or intervention that can reliably disrupt reconsolidation without requiring intracranial access for administration would be extremely useful. Electroconvulsive shock (ECS) delivered after memory retrieval has been demonstrated in some studies to disrupt memory reconsolidation; however, there exists a paucity of literature characterizing its effects on Pavlovian fear memory. Considering this, we chose to examine ECS as an inexpensive and facile means to impair reconsolidation in rats. Here we show that electroconvulsive seizure induction, when administered after memory retrieval, (immediately, after 30 min, or after 1 h), does not impair the reconsolidation of cued or contextual Pavlovian fear memories. On the contrary, ECS administration immediately after extinction training may modestly impair the consolidation of fear extinction memory.

scholarly journals Npas4 impairs fear memory via phosphorylated HDAC5 induced by CGRP administration in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Narumi Hashikawa-Hobara ◽  
Shuta Mishima ◽  
Chihiro Okujima ◽  
Youdai Shitanishi ◽  
Naoya Hashikawa
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Histone H3 ◽  
Fear Memory ◽  
Protein Kinase D ◽  
Post Traumatic Stress ◽  
Calcitonin Gene ◽  
Post Traumatic ◽  
H3 Acetylation

AbstractThe relationships among neuropeptide, calcitonin gene-related peptide (CGRP), and memory formation remain unclear. Here, we showed that the intracerebroventricular administration of CGRP impaired the traumatic fear memories, in a widely studied animal model of post-traumatic stress disorder. We found that CGRP administration suppressed fear memory by increasing neuronal PAS domain protein 4 (Npas4), phosphorylated histone deacetylase 5 (HDAC5), and protein kinase D (PKD). We also discovered that Npas4 knockdown inhibited CGRP-mediated fear memory. CGRP decreased the binding between HDAC5 and the Npas4 enhancer site and increased the binding between acetylated histone H3 and the Npas4 enhancer site. The pharmacological inhibition or knockdown of PKD attenuated the CGRP-mediated impairment of fear memory and the increased phosphorylation of HDAC5 and Npas4 expression. Our findings demonstrated that the CGRP-PKD pathway was associated with the histone H3 acetylation-Npas4 pathway. These results suggested a novel function for CGRP on fear memory, through epigenetic regulation.

scholarly journals Npas4 impairs fear memory via phosphorylated HDAC5 induced by CGRP administration in mice

2020 ◽  
Author(s):  
Narumi Hashikawa-Hobara ◽  
Shuta Mishima ◽  
Chihiro Okujima ◽  
Youdai Shitanishi ◽  
Naoya Hashikawa
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Histone H3 ◽  
Fear Memory ◽  
Protein Kinase D ◽  
Post Traumatic Stress ◽  
Calcitonin Gene ◽  
Post Traumatic ◽  
H3 Acetylation

Abstract The relationships among neuropeptide, calcitonin gene-related peptide (CGRP), and memory formation remain unclear. Here, we showed that the intracerebroventricular administration of CGRP impaired the traumatic fear memories, in a widely studied animal model of post-traumatic stress disorder. We found that CGRP administration suppressed fear memory by increasing neuronal PAS domain protein 4 (Npas4), phosphorylated histone deacetylase 5 (HDAC5), and protein kinase D (PKD). We also discovered that Npas4 knockdown inhibited CGRP-mediated fear memory. CGRP decreased the binding between HDAC5 and the Npas4 enhancer site and increased the binding between acetylated histone H3 and the Npas4 enhancer site. The pharmacological inhibition or knockdown of PKD attenuated the CGRP-mediated impairment of fear memory and the increased phosphorylation of HDAC5 and Npas4 expression. Our findings demonstrated that the CGRP-PKD pathway was associated with the histone H3 acetylation-Npas4 pathway. These results suggested a novel function for CGRP on fear memory, through epigenetic regulation.

Effects of cortisol on memory in women with borderline personality disorder: role of co-morbid post-traumatic stress disorder and major depression

2012 ◽  
Vol 43 (3) ◽  
pp. 495-505 ◽  
Author(s):  
K. Wingenfeld ◽  
M. Driessen ◽  
K. Terfehr ◽  
N. Schlosser ◽  
S. Carvalho Fernando ◽  
...  
Keyword(s):  
Working Memory ◽  
Personality Disorder ◽  
Autobiographical Memory ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Memory Retrieval ◽  
Stress Disorder ◽  
Borderline Personality ◽  
Post Traumatic Stress ◽  
Post Traumatic

BackgroundStress and cortisol administration are known to have impairing effects on memory retrieval in healthy humans. These effects are reported to be altered in patients with major depressive disorder (MDD) and post-traumatic stress disorder (PTSD) but they have not yet been investigated in borderline personality disorder (BPD).MethodIn a placebo-controlled cross-over study, 71 women with BPD and 40 healthy controls received either placebo or 10 mg of hydrocortisone orally before undertaking a declarative memory retrieval task (word list learning) and an autobiographical memory test (AMT). A working memory test was also applied.ResultsOverall, opposing effects of cortisol on memory were observed when comparing patients with controls. In controls, cortisol had impairing effects on memory retrieval whereas in BPD patients cortisol had enhancing effects on memory retrieval of words, autobiographical memory and working memory. These effects were most pronounced for specificity of autobiographical memory retrieval. Patients with BPD alone and those with co-morbid PTSD showed this effect. We also found that co-morbid MDD influenced the cortisol effects: in this subgroup (BPD + MDD) the effects of cortisol on memory were absent.ConclusionsThe present results demonstrate beneficial effects of acute cortisol elevations on hippocampal-mediated memory processes in BPD. The absence of these effects in patients with co-morbid MDD suggests that these patients differ from other BPD patients in terms of their sensitivity to glucocorticoids (GCs).

scholarly journals Fear not: recent advances in understanding the neural basis of fear memories and implications for treatment development

F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1948
Author(s):  
Amy L. Milton
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Neural Circuits ◽  
Stress Disorder ◽  
Fear Memory ◽  
Post Traumatic Stress ◽  
Neural Basis ◽  
Treatment Development ◽  
Technological Advances ◽  
Post Traumatic

Fear is a highly adaptive emotion that has evolved to promote survival and reproductive fitness. However, maladaptive expression of fear can lead to debilitating stressor-related and anxiety disorders such as post-traumatic stress disorder. Although the neural basis of fear has been extensively researched for several decades, recent technological advances in pharmacogenetics and optogenetics have allowed greater resolution in understanding the neural circuits that underlie fear. Alongside conceptual advances in the understanding of fear memory, this increased knowledge has clarified mechanisms for some currently available therapies for post-traumatic stress disorder and has identified new potential treatment targets.

scholarly journals Shifting from fear to safety through deconditioning-update

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Bruno Popik ◽  
Felippe Espinelli Amorim ◽  
Olavo B Amaral ◽  
Lucas De Oliveira Alvares
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Memory Retrieval ◽  
Stress Disorder ◽  
Behavioral Approach ◽  
Post Traumatic Stress ◽  
Memory Updating ◽  
Traumatic Memories ◽  
Voltage Gated Calcium Channels ◽  
Post Traumatic

Aversive memories are at the heart of psychiatric disorders such as phobias and post-traumatic stress disorder (PTSD). Here, we present a new behavioral approach in rats that robustly attenuates aversive memories. This method consists of ‘deconditioning’ animals previously trained to associate a tone with a strong footshock by replacing it with a much weaker one during memory retrieval. Our results indicate that deconditioning-update is more effective than traditional extinction in reducing fear responses; moreover, such effects are long lasting and resistant to renewal and spontaneous recovery. Remarkably, this strategy overcame important boundary conditions for memory updating, such as remote or very strong traumatic memories. The same beneficial effect was found in other types of fear-related memories. Deconditioning was mediated by L-type voltage-gated calcium channels and is consistent with computational accounts of mismatch-induced memory updating. Our results suggest that shifting from fear to safety through deconditioning-update is a promising approach to attenuate traumatic memories.

scholarly journals Characterizing changes in glucocorticoid receptor internalization in the fear circuit in an animal model of post traumatic stress disorder

2018 ◽  
Author(s):  
Emly Moulton ◽  
Marisa Chamness ◽  
Dayan Knox
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Glucocorticoid Receptors ◽  
Stress Disorder ◽  
Dorsal Hippocampus ◽  
Fear Memory ◽  
Receptor Internalization ◽  
Post Traumatic Stress ◽  
Post Traumatic ◽  
Individual Nodes

AbstractGlucocorticoid receptors (GRs) shuttle from the cytoplasm (cy) to the nucleus (nu) when bound with glucocorticoids (i.e. GR internalization) and alter transcriptional activity. GR activation within the fear circuit has been implicated in fear memory and post traumatic stress disorder (PTSD). However, no study to date has characterized GR internalization within the fear circuit during fear memory formation or examined how traumatic stress impacts this process. To address this, we assayed cy and nu GR levels at baseline and after auditory fear conditioning (FC) in the single prolonged stress (SPS) model of PTSD. Cy and nu GRs within the medial prefrontal cortex (mPFC), dorsal hippocampus (dHipp), ventral hippocampus (vHipp), and amygdala (AMY) were assayed using western blot. The distribution of GR in the cy and nu (at baseline and after FC) was varied across individual nodes of the fear circuit. At baseline, SPS enhanced cyGRs in the dHipp, but decreased cyGRs in the AMY. FC only enhanced GR internalization in the AMY and this effect was attenuated by SPS exposure. SPS also decreased cyGRs in the dHipp after FC. The results of this study suggests that GR internalization is varied across the fear circuit, which in turn suggests GR activation is selectively regulated within individual nodes of the fear circuit. The findings also suggest that changes in GR dynamics in the dHipp and AMY modulate the enhancing effect SPS has on fear memory persistence.

Brexpiprazole blocks post-traumatic stress disorder-like memory while promoting normal fear memory

2020 ◽  
Author(s):  
Eva-Gunnel Ducourneau ◽  
Christelle Guette ◽  
Damien Perrot ◽  
Miguel Mondesir ◽  
Cédric Mombereau ◽  
...  
Keyword(s):  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Fear Memory ◽  
Post Traumatic Stress ◽  
Post Traumatic
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