0
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      Corticosterone impairs gap junctions in the prefrontal cortical and hippocampal astrocytes via different mechanisms.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Increasing evidence has implicated astrocyte pathology in the etiopathology of major depressive disorder (MDD). In particular, dysfunction of gap junctions in astrocytes is a potential target for MDD treatment. However, the mechanism underlying stress-induced dysfunction of gap junctions is still unknown. We therefore studied the mechanism of stress-induced dysfunction of gap junctions in prefrontal cortical and hippocampal astrocytes. Corticosterone (CORT) was used to induce stress conditions; CORT damaged the function of gap junctions, which resulted from less distribution of connexin43 (Cx43) on membranes and the enhanced phosphorylation of Cx43 at S368. Moreover, CORT downregulated the biosynthesis of Cx43 but increased the degradation of Cx43. Interestingly, both autophagy and the proteasome system were involved in the degradation of Cx43 in prefrontal cortical astrocytes, but only the proteasome system was involved in the degradation of Cx43 in hippocampal astrocytes. CORT significantly induced the formation of annular gap junction vesicles in prefrontal cortical astrocytes; however, Cx43 mainly presented as small dots in the hippocampal astrocytes. Furthermore, CORT increased N-Cadherin expression and the interactions of Cx43 with ZO-1/drebrin in prefrontal cortical astrocytes, but these interactions were oppositely modulated in hippocampal astrocytes. In conclusion, this study clarified the alternations of the Cx43 life cycle in the prefrontal cortical and hippocampal astrocytes exposed to CORT, which may contribute to our understanding of the mechanisms underlying stress-induced dysfunction of gap junctions.

          Related collections

          Author and article information

          Journal
          Neuropharmacology
          Neuropharmacology
          Elsevier BV
          1873-7064
          0028-3908
          March 15 2018
          : 131
          Affiliations
          [1 ] State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica & Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
          [2 ] Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510000, China.
          [3 ] College of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China.
          [4 ] State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica & Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, 510000, China; College of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China. Electronic address: chennh@imm.ac.cn.
          Article
          S0028-3908(17)30592-0
          10.1016/j.neuropharm.2017.12.003
          29223529
          32743ed7-109b-48f0-bcc7-6bdcba7da844

          Corticosterone,Gap junction,Astrocyte,Connexin43,Depression
          Corticosterone, Gap junction, Astrocyte, Connexin43, Depression

          Comments

          Comment on this article