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

التفاصيل البيبلوغرافية
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
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
الوصف
تدمد:14220067
16616596
DOI:10.3390/ijms24032303