دورية أكاديمية
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: | Fernando Yáñez-Gómez, Alfredo Ramos-Miguel, Jesús A. García-Sevilla, Jorge Manzanares, Teresa Femenía |
المصدر: | International Journal of Molecular Sciences, Vol 24, Iss 3, p 2303 (2023) |
بيانات النشر: | MDPI AG, 2023. |
سنة النشر: | 2023 |
المجموعة: | LCC:Biology (General) LCC:Chemistry |
مصطلحات موضوعية: | prodynorphin, JNK, ERK, chronic mild stress, apoptosis, phosphorylation, Biology (General), QH301-705.5, Chemistry, QD1-999 |
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. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 1422-0067 1661-6596 |
العلاقة: | https://www.mdpi.com/1422-0067/24/3/2303Test; https://doaj.org/toc/1661-6596Test; https://doaj.org/toc/1422-0067Test |
DOI: | 10.3390/ijms24032303 |
الوصول الحر: | https://doaj.org/article/94b58504fc934ab298b046e5892cc72bTest |
رقم الانضمام: | edsdoj.94b58504fc934ab298b046e5892cc72b |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 14220067 16616596 |
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DOI: | 10.3390/ijms24032303 |