ArticleFrontiers in behavioral neuroscience2017
Change of Rin1 and Stathmin in the Animal Model of Traumatic Stresses.
Article in Frontiers in behavioral neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Systematic Review and Methodological Considerations for the Use of Single Prolonged Stress and Fear Extinction Retention in Rodents.Frontiers in behavioral neuroscience · 2021Pooled it
- Use of Single Prolonged Stress to Model Post-traumatic Stress Disorder in Rodents: What We Found and Where to Next?Current neuropharmacology · 2026Review
- Effects of Social Defeat Stress on Microtubule Regulating Proteins and Tubulin Polymerization.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024Article
- Stress-related cellular pathophysiology as a crosstalk risk factor for neurocognitive and psychiatric disorders.BMC neuroscience · 2023Review
- What Happened in the Hippocampal Axon in a Rat Model of Posttraumatic Stress Disorder.Cellular and molecular neurobiology · 2022Article
- Impact of Social Defeat Stress on DNA Methylation in Drd2, Nr3c1, and Stmn1 in Wild-type and Stmn1 Knock-out Mice.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2022Article
- Myelination defects in the medial prefrontal cortex of Fkbp5 knockout mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Stathmin Regulates Spatiotemporal Variation in the Memory Loop in Single-Prolonged Stress Rats.Journal of molecular neuroscience : MN · 2020Article
- Effects ofBrain sciences · 2019Article
- Clinical Therapeutic Strategy and Neuronal Mechanism Underlying Post-Traumatic Stress Disorder (PTSD).International journal of molecular sciences · 2019Review
- Traumatic Stress Produces Distinct Activations of GABAergic and Glutamatergic Neurons in Amygdala.Frontiers in neuroscience · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanism of fear memory is poorly understood. Therefore, the pathogenesis of post-traumatic stress disorder (PTSD), whose symptom presentation can enhance fear memory, remains largely unclear. Recent studies with knockout animals have reported that Rin1 and stathmin regulate fear memory. Rin1 inhibits acquisition and promotes memory extinction, whereas stathmin regulates innate and basal fear. The aim of our study was to examine changes in the expression of Rin1 and stathmin in different animal models of stress, particluarly traumatic stress. We used three animal traumatic stresses: single prolonged stress (SPS, which is a rodent model of PTSD), an immobilization-stress (IM) and a Loud sound stress (LSS), to examine the change and uniqueness in Rin1/stathmin expression. Behavioral tests of SPS rats demonstrated increased anxiety and contextual fear-conditioning. They showed decreased long-term potentiation (LTP), as well as decreased stathmin and increased Rin1 expression in the hippocampus and the amygdala. Expression of the stathmin effector, tubulin, and downstream molecules Rin1, Rab5, and Abl, appeared to increase. Rin1 and EphA4 were endogenously coexpressed in primary neurons after SPS stimulation. IM rats exhibited increased anxiety behavior and enhanced fear-conditioning to contextual and auditory stimuli. Similar changes in expression of Rin1/stathmin were observed in IM rats whereas no changes were observed in rats exposed to a loud sound. These data suggest that changes in expression of the Rin1 and stathmin genes may be involved in rodents with SPS and IM stresses, which provide valuable insight into fear memories under abnormal conditions, particularly in PTSD.
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