Academic Journal
Regulation of Cortico-Thalamic JNK1/2 and ERK1/2 MAPKs and Apoptosis-Related Signaling Pathways in PDYN Gene-Deficient Mice Following Acute and Chronic Mild Stress
| العنوان: | Regulation of Cortico-Thalamic JNK1/2 and ERK1/2 MAPKs and Apoptosis-Related Signaling Pathways in PDYN Gene-Deficient Mice Following Acute and Chronic Mild Stress |
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| المؤلفون: | Yáñez Gómez, Fernando, Ramos Miguel, Alfredo, García Sevilla, Jesús A., Manzanares, Jorge, Femenía, Teresa |
| بيانات النشر: | MDPI |
| سنة النشر: | 2023 |
| المجموعة: | ADDI: Repositorio Institucional de la Universidad del País Vasco / Euskal Herriko Unibertsitatea (UPV/EHU - Basque Country University) |
| مصطلحات موضوعية: | prodynorphin, JNK, ERK, chronic mild stress, apoptosis, phosphorylation |
| الوصف: | The crosstalk between the opioidergic system and mitogen-activated protein kinases (MAPKs) has a critical role in mediating stress-induced behaviors related to the pathophysiology of anxiety. The present study evaluated the basal status and stress-induced alterations of cortico-thalamic MAPKs and other cell fate-related signaling pathways potentially underlying the anxiogenic endophenotype of PDYN gene-deficient mice. Compared to littermates, PDYN knockout (KO) mice had lower cortical and or thalamic amounts of the phospho-activated MAPKs c-Jun N-terminal kinase (JNK1/2) and extracellular signal-regulated kinase (ERK1/2). Similarly, PDYN-KO animals displayed reduced cortico-thalamic densities of total and phosphorylated (at Ser191) species of the cell fate regulator Fas-associated protein with death domain (FADD) without alterations in the Fas receptor. Exposure to acute restraint and chronic mild stress stimuli induced the robust stimulation of JNK1/2 and ERK1/2 MAPKs, FADD, and Akt-mTOR pathways, without apparent increases in apoptotic rates. Interestingly, PDYN deficiency prevented stress-induced JNK1/2 and FADD but not ERK1/2 or Akt-mTOR hyperactivations. These findings suggest that cortico-thalamic MAPK- and FADD-dependent neuroplasticity might be altered in PDYN-KO mice. In addition, the results also indicate that the PDYN gene (and hence dynorphin release) may be required to stimulate JNK1/2 and FADD (but not ERK1/2 or Akt/mTOR) pathways under environmental stress conditions. ; This joint research was funded by Red Temática de Investigación Cooperativa en Salud–Red de Trastornos Adictivos (RETICS–RTA, Instituto de Salud Carlos III [ISCIII], MCIU/AEI/FEDER), Grupos RD06/0001/0004 (J.M.) and RD06/0001/0003 (J.A.G.-S.). J.M. also received financial support from Proyectos de Investigación en Salud—ISCIII (grant RD. PI18/00576), Red de Investigación en Atención Primaria de Adicciones (grant RD21/0009/0008), and Delegación del Gobierno para el Plan Nacional Sobre Drogas (PNSD, grant 2019I012) from the Spanish ... |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | application/pdf |
| اللغة: | English |
| تدمد: | 1422-0067 |
| Relation: | info:eu-repo/grantAgreement/MICIU/RTI2018-094414-A-I00; info:eu-repo/grantAgreement/MICINN/PID2019-109323RA-I00; info:eu-repo/grantAgreement/MICINN/SAF2008-01311; info:eu-repo/grantAgreement/MINECO/RYC-2016-19282; info:eu-repo/grantAgreement/MINECO/RYC-2017-22666; https://www.mdpi.com/1422-0067/24/3/2303; International Journal of Molecular Sciences 24(3) : (2023) // Article ID 2303; http://hdl.handle.net/10810/59788 |
| DOI: | 10.3390/ijms24032303 |
| الاتاحة: | http://hdl.handle.net/10810/59788 https://doi.org/10.3390/ijms24032303 |
| Rights: | info:eu-repo/semantics/openAccess ; http://creativecommons.org/licenses/by/4.0/es/ ; © 2023 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/ 4.0/). |
| رقم الانضمام: | edsbas.46EF3203 |
| قاعدة البيانات: | BASE |
Full Text Finder | تدمد: | 14220067 |
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| DOI: | 10.3390/ijms24032303 |