trans-Resveratrol ameliorates anxiety-like behaviors and fear memory deficits in a rat model of post-traumatic stress disorder

2018 ◽  
Vol 133 ◽  
pp. 181-188 ◽  
Author(s):  
Gaowen Li ◽  
Gang Wang ◽  
Jing Shi ◽  
Xueyi Xie ◽  
Ning Fei ◽  
...  
Keyword(s):  
Rat Model ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Memory Deficits ◽  
Fear Memory ◽  
Post Traumatic Stress ◽  
Post Traumatic

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.

scholarly journals Selective dopamine D3 receptor antagonism significantly attenuates stress-induced immobility in a rat model of post-traumatic stress disorder

Synapse ◽  
2018 ◽  
Vol 72 (8) ◽  
pp. e22035 ◽  
Author(s):  
Onarae V. Rice ◽  
Charles R. Ashby ◽  
Clark Dixon ◽  
William Laurenzo ◽  
Jason Hayden ◽  
...  
Keyword(s):  
Rat Model ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Stress Disorder ◽  
Dopamine D3 Receptor ◽  
D3 Receptor ◽  
Post Traumatic Stress ◽  
Dopamine D3 ◽  
Post Traumatic ◽  
Selective Dopamine

scholarly journals Omega-3 Fatty Acids Prevent Post-Traumatic Stress Disorder-Induced Memory Impairment

Biomolecules ◽  
2019 ◽  
Vol 9 (3) ◽  
pp. 100 ◽  
Author(s):  
Laiali Alquraan ◽  
Karem H. Alzoubi ◽  
Hana Hammad ◽  
Suzie Y. Rababa’h ◽  
Fadia Mayyas
Keyword(s):  
Fatty Acids ◽  
Rat Model ◽  
Post Traumatic Stress Disorder ◽  
Traumatic Stress ◽  
Memory Impairment ◽  
Stress Disorder ◽  
Omega 3 Fatty Acids ◽  
Omega 3 ◽  
Post Traumatic Stress ◽  
Post Traumatic

Post-traumatic stress disorder (PTSD) is a psychiatric disorder that can happen after exposure to a traumatic event. Post-traumatic stress disorder is common among mental health disorders that include mood and anxiety disorders. Omega-3 fatty acids (OMGs) are essential for the maintenance of brain function and prevention of cognition dysfunctions. However, the possible effect of OMG on memory impairment induced by PTSD has not been studied. In here, such an effect was explored using a rat model of PTSD. The PTSD-like behavior was induced in animals using a single-prolonged stress (SPS) rat model of PTSD (2 h restraint, 20 min forced swimming, 15 min rest, 1–2 min diethyl ether exposure). The OMG was administered orally at a dose of 100 mg omega-3 polyunsaturated fatty acid (PUFA)/100 g body weight/day. Spatial learning and memory were assessed using the radial arm water maze (RAWM) method. Changes in oxidative stress biomarkers, thiobarbituric acid reactive substances (TBARS), and brain derived neuroptrophic factor (BDNF) in the hippocampus following treatments were measured. The results revealed that SPS impaired both short- and long-term memory (p < 0.05). Use of OMG prevented memory impairment induced by SPS. Furthermore, OMG normalized SPS induced changes in the hippocampus that reduced glutathione (GSH), oxidized glutathione (GSSG), GSH/GSSG ratios, the activity of catalase, glutathione peroxidase (GPx), and TBARSs levels. In conclusion, the SPS model of PTSD-like behavior generated memory impairment, whereas OMG prevented this impairment, possibly through normalizing antioxidant mechanisms in the hippocampus.

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.

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