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Inhibition of Protein Synthesis Attenuates Formation of Traumatic Memory and Normalizes Fear-Induced c-Fos Expression in a Mouse Model of Posttraumatic Stress Disorder.

التفاصيل البيبلوغرافية
العنوان: Inhibition of Protein Synthesis Attenuates Formation of Traumatic Memory and Normalizes Fear-Induced c-Fos Expression in a Mouse Model of Posttraumatic Stress Disorder.
المؤلفون: Zamorina TA; Institute for Advanced Brain Studies, Lomonosov Moscow State University, 119991 Moscow, Russia.; Faculty of Biology, Department of Higher Nervous Activity, Lomonosov Moscow State University, 119234 Moscow, Russia., Ivashkina OI; Institute for Advanced Brain Studies, Lomonosov Moscow State University, 119991 Moscow, Russia.; Laboratory of Neuronal Intelligence, Lomonosov Moscow State University, 119991 Moscow, Russia., Toropova KA; Institute for Advanced Brain Studies, Lomonosov Moscow State University, 119991 Moscow, Russia.; Laboratory of Neuronal Intelligence, Lomonosov Moscow State University, 119991 Moscow, Russia., Anokhin KV; Institute for Advanced Brain Studies, Lomonosov Moscow State University, 119991 Moscow, Russia.; Laboratory of Neuronal Intelligence, Lomonosov Moscow State University, 119991 Moscow, Russia.
المصدر: International journal of molecular sciences [Int J Mol Sci] 2024 Jun 13; Vol. 25 (12). Date of Electronic Publication: 2024 Jun 13.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: MDPI Country of Publication: Switzerland NLM ID: 101092791 Publication Model: Electronic Cited Medium: Internet ISSN: 1422-0067 (Electronic) Linking ISSN: 14220067 NLM ISO Abbreviation: Int J Mol Sci Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Basel, Switzerland : MDPI, [2000-
مواضيع طبية MeSH: Fear* , Memory* , Proto-Oncogene Proteins c-fos*/metabolism , Stress Disorders, Post-Traumatic*/metabolism, Animals ; Male ; Mice ; Brain/metabolism ; Disease Models, Animal ; Mice, Inbred C57BL ; Protein Biosynthesis ; Protein Synthesis Inhibitors/pharmacology
مستخلص: Posttraumatic stress disorder (PTSD) is a debilitating psychosomatic condition characterized by impairment of brain fear circuits and persistence of exceptionally strong associative memories resistant to extinction. In this study, we investigated the neural and behavioral consequences of inhibiting protein synthesis, a process known to suppress the formation of conventional aversive memories, in an established PTSD animal model based on contextual fear conditioning in mice. Control animals were subjected to the conventional fear conditioning task. Utilizing c-Fos neural activity mapping, we found that the retrieval of PTSD and normal aversive memories produced activation of an overlapping set of brain structures. However, several specific areas, such as the infralimbic cortex and the paraventricular thalamic nucleus, showed an increase in the PTSD group compared to the normal aversive memory group. Administration of protein synthesis inhibitor before PTSD induction disrupted the formation of traumatic memories, resulting in behavior that matched the behavior of mice with usual aversive memory. Concomitant with this behavioral shift was a normalization of brain c-Fos activation pattern matching the one observed in usual fear memory. Our findings demonstrate that inhibiting protein synthesis during traumatic experiences significantly impairs the development of PTSD in a mouse model. These data provide insights into the neural underpinnings of protein synthesis-dependent traumatic memory formation and open prospects for the development of new therapeutic strategies for PTSD prevention.
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معلومات مُعتمدة: Non-Commercial Foundation for Support of Science and Education "INTELLECT".
فهرسة مساهمة: Keywords: c-Fos; cycloheximide; fear conditioning; posttraumatic stress disorder; protein synthesis
المشرفين على المادة: 0 (Protein Synthesis Inhibitors)
0 (Proto-Oncogene Proteins c-fos)
تواريخ الأحداث: Date Created: 20240627 Date Completed: 20240627 Latest Revision: 20240722
رمز التحديث: 20240722
مُعرف محوري في PubMed: PMC11204086
DOI: 10.3390/ijms25126544
PMID: 38928250
قاعدة البيانات: MEDLINE
الوصف
تدمد:1422-0067
DOI:10.3390/ijms25126544