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Contextual fear

Shuhua Lai, Gangwei Wu, Zhixian Jiang
BACKGROUND/AIMS: Impaired fear memory extinction is widely considered a key mechanism of post-traumatic stress disorder (PTSD). Recent studies have suggested that neuroinflammation after a single prolonged stress (SPS) exposure may play a critical role in the impaired fear memory extinction. Studies have shown that high mobility group box chromosomal protein 1 (HMGB-1) is critically involved in neuroinflammation. However, the role of HMGB-1 underlying the development of impairment of fear memory extinction is still not known...
March 16, 2018: Cellular Physiology and Biochemistry
Mohammad Shehata, Kareem Abdou, Kiriko Choko, Mina Matsuo, Hirofumi Nishizono, Kaoru Inokuchi
There is substantial interest in memory reconsolidation as a target for the treatment of anxiety disorders such as post-traumatic stress disorder (PTSD). However, its applicability is restricted by reconsolidation-resistant boundary conditions that constrain the initial memory destabilization. In this study, we investigated whether the induction of synaptic protein degradation through autophagy modulation, a major protein degradation pathway, can enhance memory destabilization upon retrieval and whether it can be utilized to overcome these conditions...
March 19, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Mariana Fortunata Donadon, Rocio Martin-Santos, Flávia de Lima Osório
Studies have shown that traumatic experiences may affect hormonal systems mediated by the hypothalamic-pituitary-adrenal (HPA) axis and the oxytocinergic system. This effect is the result of long-term impairments in hypothalamic structures and negative feedback mechanisms within the HPA axis, structures that mediate the response to stress. This deregulation reduces the production and release of cortisol and oxytocin (OXT), which may alter stress responses and lead to increased vulnerability to impairments from stressful experiences...
2018: Frontiers in Pharmacology
Daniel M Stout, Daniel E Glenn, Dean T Acheson, Andrea D Spadoni, Victoria B Risbrough, Alan N Simmons
Contextual threat learning reflects two often competing processes: configural and elemental learning. Configural threat learning is a hippocampal-dependent process of forming a conjunctive representation of a context through binding of several multi-modal elements. In contrast, elemental threat-learning is governed by the amygdala and involves forming associative relationships between individual features within the context. Contextual learning tasks in humans however, rarely probe if a learned fear response is truly due to configural learning vs...
March 12, 2018: Neurobiology of Learning and Memory
Caroline Morel, Tessi Sherrin, Norman J Kennedy, Kelly H Forest, Seda Avcioglu Barutcu, Michael Robles, Ezekiel Carpenter-Hyland, Naghum Alfulaij, Claire L Standen, Robert A Nichols, Morris Benveniste, Roger J Davis, Cedomir Todorovic
The c-Jun N-terminal kinase (JNK) signal transduction pathway is implicated in learning and memory. Here, we examined the role of JNK activation mediated by the JIP1 scaffold protein. We compared male wild-type mice with a mouse model harboring a point mutation in the Jip1 gene that selectively blocks JIP1-mediated JNK activation. These male mutant mice exhibited increased NMDA receptor currents, increased NMDA receptor-mediated gene expression, and a lower threshold for induction of hippocampal long-term potentiation...
March 14, 2018: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Marion Waite, Clare Martin, Rachel Franklin, David Duce, Rachel Harrison
BACKGROUND: People with type 1 diabetes (T1D) undertake self-management to prevent short and long-term complications. Advanced technology potentially supports such activities but requires consideration of psychological and behavioral constructs and usability issues. Economic factors and health care provider capacity influence access and uptake of advanced technology. Previous reviews have focused upon clinical outcomes or were descriptive or have synthesized studies on adults with those on children and young people where human factors are different...
March 15, 2018: JMIR Human Factors
Shingo Matsuda, Daisuke Matsuzawa, Daisuke Ishii, Haruna Tomizawa, Eiji Shimizu
Onset of fear-related disorders such as post-traumatic stress disorder is enhanced from adolescence until adulthood. However, the biological mechanisms underlying this vulnerability remain unclear. Therefore, we investigated contextual fear memory and extinction in 4-, 6-, 8-, 10-, and 15-week-old female mice. We also measured phosphorylation of ERK2 in the medial prefrontal cortex (mPFC) and the dorsal hippocampus in the mPFC following fear conditioning or extinction in 6- and 15-week-old mice. We found that 10- and 15-week-old mice showed stronger fear memory and more resistance to fear extinction than 6-week-old mice...
March 10, 2018: Neurobiology of Learning and Memory
Ki Eun Shin, Michelle G Newman
Even after successful exposure, relapse is not uncommon. Based on the retrieval model of fear extinction (e.g., Vervliet, Craske, & Hermans, 2013), return of fear can occur after exposure due to an elapse of time (spontaneous recovery) or change in context (contextual renewal). The use of external salient stimuli presented throughout extinction (i.e., retrieval cues [RCs]) has been suggested as a potential solution to this problem (Bouton, 2002). The current study examined whether RCs attenuated return of fear in individuals with public speaking anxiety...
March 2018: Behavior Therapy
Jeanie K Meckes, Patrick H Lim, Stephanie L Wert, Wendy Luo, Stephanie A Gacek, Dana Platt, Ryan Jankord, Kathrin Saar, Eva E Redei
Acute stress responsiveness is a quantitative trait that varies in severity from one individual to another; however, the genetic component underlying the individual variation is largely unknown. Fischer 344 (F344) and Wistar Kyoto (WKY) rat strains show large differences in behavioral responsiveness to acute stress, such as freezing behavior in response to footshock during the conditioning phase of contextual fear conditioning (CFC). Quantitative trait loci (QTL) have been identified for behavioral responsiveness to acute stress in the defensive burying (DB) and open field test (OFT) from a reciprocal F2 cross of F344 and WKY rat strains...
2018: PloS One
Nannan Guo, Marta E Soden, Charlotte Herber, Michael TaeWoo Kim, Antoine Besnard, Paoyan Lin, Xiang Ma, Constance L Cepko, Larry S Zweifel, Amar Sahay
Memories become less precise and generalized over time as memory traces reorganize in hippocampal-cortical networks. Increased time-dependent loss of memory precision is characterized by an overgeneralization of fear in individuals with post-traumatic stress disorder (PTSD) or age-related cognitive impairments. In the hippocampal dentate gyrus (DG), memories are thought to be encoded by so-called 'engram-bearing' dentate granule cells (eDGCs). Here we show, using rodents, that contextual fear conditioning increases connectivity between eDGCs and inhibitory interneurons (INs) in the downstream hippocampal CA3 region...
March 12, 2018: Nature Medicine
Mirelle A Casagrande, Josué Haubrich, Lizeth K Pedraza, Bruno Popik, Jorge A Quillfeldt, Lucas de Oliveira Alvares
Memories are not instantly created in the brain, requiring a gradual stabilization process called consolidation to be stored and persist in a long-lasting manner. However, little is known whether this time-dependent process is dynamic or static, and the factors that might modulate it. Here, we hypothesized that the time-course of consolidation could be affected by specific learning parameters, changing the time window where memory is susceptible to retroactive interference. In the rodent contextual fear conditioning paradigm, we compared weak and strong training protocols and found that in the latter memory is susceptible to post-training hippocampal inactivation for a shorter period of time...
March 5, 2018: Neurobiology of Learning and Memory
Dake Song, Yaping Ge, Zhaodi Chen, Chao Shang, Ying Guo, Taiyun Zhao, Yunfeng Li, Ning Wu, Rui Song, Jin Li
Post-traumatic stress disorder (PTSD) is a complicated psychiatric disorder, which occurs after exposure to a traumatic event. The main clinical manifestation of PTSD includes fear and stress dysregulation. In both animals and humans, dysregulation of dopamine function appears to be related to conditioned fear responses. Previous studies show that the dopamine D3 receptor (D3R) is involved in schizophrenia, autism, and substance use disorders and is related to emotional disorders. However, few studies have investigated the role of the D3R in the pathogenesis and aetiology of PTSD...
March 3, 2018: Progress in Neuro-psychopharmacology & Biological Psychiatry
Floortje B Moes, Eddy S Houwaart, Diana M J Delnoij, Klasien Horstman
RATIONALE, AIMS, AND OBJECTIVES: This paper examines a remarkable dispute between Dutch insurers, hospitals, doctors, and patients about a set of quality indicators. In 2013, private insurers planned to drastically reform Dutch emergency care using quality indicators they had formulated drawing from clinical guidelines, RCTs, and systematic reviews. Insurers' plans caused much debate in the field of emergency care. As quality indicators have come to play a more central role in health care governance, the questions what constitutes good evidence for them, how they ought to be used, and who controls them have become politically and morally charged...
March 6, 2018: Journal of Evaluation in Clinical Practice
Linda Marschner, An Schreurs, Benoit Lechat, Jesper Mogensen, Anton Roebroek, Tariq Ahmed, Detlef Balschun
Mild traumatic brain injury (mTBI) can lead to diffuse neurophysical damage as well as cognitive and affective alterations. The nature and extent of behavioral changes after mTBI are still poorly understood and how strong an impact force has to be to cause long-term behavioral changes is not yet known. Here, we examined spatial learning acquisition, retention and reversal in a Morris water maze, and assessed search strategies during task performance after a single, mild, closed-skull traumatic impact referred to as "minimal" TBI...
February 27, 2018: Behavioural Brain Research
Munir Gunes Kutlu, Robert D Cole, David A Connor, Brendan Natwora, Thomas J Gould
Anxiety and stress disorders have been linked to deficits in fear extinction. Our laboratory and others have demonstrated that acute nicotine impairs contextual fear extinction, suggesting that nicotine exposure may have negative effects on anxiety and stress disorder symptomatology. However, the neurobiological mechanisms underlying the acute nicotine-induced impairment of contextual fear extinction are unknown. Therefore, based on the previous studies showing that brain-derived neurotrophic factor is central for fear extinction learning and acute nicotine dysregulates brain-derived neurotrophic factor signaling, we hypothesized that the nicotine-induced impairment of contextual fear extinction may involve changes in tyrosine receptor kinase B signaling...
February 1, 2018: Journal of Psychopharmacology
Patrick H Lim, Stephanie L Wert, Elif Tunc-Ozcan, Robert Marr, Adriana Ferreira, Eva E Redei
Aging and major depressive disorder are risk factors for dementia, including Alzheimer's Disease (AD), but the mechanism(s) linking depression and dementia are not known. Both AD and depression show greater prevalence in women. We began to investigate this connection using females of the genetic model of depression, the inbred Wistar Kyoto More Immobile (WMI) rat. These rats consistently display depression-like behavior compared to the genetically close control, the Wistar Kyoto Less Immobile (WLI) strain. Hippocampus-dependent contextual fear memory did not differ between young WLI and WMI females, but, by middle-age, female WMIs showed memory deficits compared to same age WLIs...
February 25, 2018: Behavioural Brain Research
Nathalie Alvarez-Ricartes, Patricia Oliveros-Matus, Cristhian Mendoza, Nelson Perez-Urrutia, Florencia Echeverria, Alexandre Iarkov, George E Barreto, Valentina Echeverria
Failure in fear extinction is one of the more troublesome characteristics of posttraumatic stress disorder (PTSD). Cotinine facilitates fear memory extinction and reduces depressive-like behavior when administered 24 h after fear conditioning in mice. In this study, it was investigated the behavioral and molecular effects of cotinine, and other antidepressant preparations infused intranasally. Intranasal (IN) cotinine, IN krill oil, IN cotinine plus krill oil, and oral sertraline were evaluated on depressive-like behavior and fear retention and extinction after fear conditioning in C57BL/6 mice...
February 27, 2018: Molecular Neurobiology
Rong-Ting Zhu, Xiang-Hui Liu, Yan-Wei Shi, Xiao-Guang Wang, Li Xue, Hu Zhao
Introduction: One hallmark symptom of post-traumatic stress disorder (PTSD) is an inability to restrict fear responses to the appropriate predictor. An infusion of glucocorticoids (GCs) after a high-intensity shock has been shown to induce PTSD-like memory impairments. In addition to GCs, noradrenergic signalling is also recognized as a key biomarker underlying PTSD symptomatology. Methods: To explore the role of the noradrenergic system in PTSD-like memory impairments, in this study, various doses of the β-adrenoceptor antagonist propranolol were systemically or bilaterally injected into the dorsal hippocampus immediately after unpaired cue-shock contextual fear conditioning, and then the rats were tested 24 h later...
February 2018: Brain and Behavior
Sharon S Lander, Usman Khan, Nicole Lewandowski, Darpan Chakraborty, Frank A Provenzano, Susana Mingote, Sergiy Chornyy, Francesca Frigerio, Pierre Maechler, Hanoch Kaphzan, Scott A Small, Stephen Rayport, Inna Gaisler-Salomon
Brain imaging has revealed that the CA1 subregion of the hippocampus is hyperactive in prodromal and diagnosed patients with schizophrenia (SCZ), and that glutamate is a driver of this hyperactivity. Strikingly, mice deficient in the glutamate synthetic enzyme glutaminase have CA1 hypoactivity and a SCZ-resilience profile, implicating glutamate-metabolizing enzymes. To address this further, we examined mice with a brain-wide deficit in the glutamate-metabolizing enzyme glutamate dehydrogenase (GDH), encoded by Glud1, which should lead to glutamate excess due to reduced glutamate metabolism in astrocytes...
February 20, 2018: Schizophrenia Bulletin
Olena Bukalo, Andrew Holmes
In this issue of Neuron, Rozeske et al. (2018) use an ingenuous behavioral paradigm to change pertinent sensory stimuli defining a given context to interrogate how the dorsomedial prefrontal cortex (dmPFC) and periaqueductal gray (PAG) interact during contextual fear discrimination.
February 21, 2018: Neuron
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