For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
18
views
28
references
 Top references
cited by
1
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      308
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      CaMK II γ down regulation protects dorsal root ganglion neurons from ropivacaine hydrochloride neurotoxicity

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      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

          T-type calcium channels are intimately involved in the local anesthetics neurotoxicity. Does CaMKIIγ regulate T-type calcium currents in local anesthetics neurotoxicity? This study generated pAd-CaMKIIγ and pAd-shRNA adenovirus vectors to up- and down-regulate CaMKIIγ mRNA expression in dorsal root ganglion neurons (DRG). Normal DRG (Normal group), empty vector DRG (Empty vector group), pAd-CaMKIIγ DRG (pAd-CaMKIIγ group) and pAd-shRNA DRG (pAd-shRNA group) were treated or untreated with 3 mM ropivacaine hydrochloride for 4 h. Cell viability, apoptosis rate, CaMKIIγ, pCaMKIIγ, Cav3.2, and Cav3.3 expression were detected. Ultrastructural changes in DRG were observed under a transmission electron microscope. The results demonstrated that the cell viability of DRG treated with ropivacaine hydrochloride decreased markedly, the apoptosis rate, CaMKIIγ, pCaMKIIγ, Cav3.2, Cav3.3 expression increased significantly. CaMKIIγ up-regulation aggravated ropivacaine hydrochloride-induced cell damage and increased Cav3.2 and Cav3.3 expression. In conclusion, CaMKIIγ regulated Cav3.2 and Cav3.3 expression in DRG, which was involved with ropivacaine hydrochloride-induced cell injury.

          Related collections

          Most cited references28

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Calcium/calmodulin-dependent kinase II and Alzheimer’s disease

          Anshua Ghosh, Karl Giese (2015)
          CaMKII is a remarkably complex protein kinase, known to have a fundamental role in synaptic plasticity and memory formation. Further, CaMKII has also been suggested to be a tau kinase. CaMKII dysregulation may therefore be a modulator of toxicity in Alzheimer’s disease, a dementia characterised by aberrant calcium signalling, synapse and neuronal loss, and impaired memory. Here, we first examine the evidence for CaMKII dysregulation in Alzheimer’s patients and draw parallels to findings in disease models which recapitulate key aspects of the disease. We then put forward the hypothesis that these changes critically contribute to neurodegeneration and memory impairment in Alzheimer’s disease.
          Article 0 comments Cited 57 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Neuronal excitability and calcium/calmodulin-dependent protein kinase type II: location, location, location.

            Xiao Liu, Graham K. Murray (2012)
            Calcium/calmodulin-dependent protein kinase type II (CaMKII) is a highly abundant serine/threonine kinase comprising a significant fraction of total protein in mammalian forebrain and forming a major component of the postsynaptic density. CaMKII is essential for certain forms of synaptic plasticity and memory consolidation and this is mediated through substrate binding and intramolecular phosphorylation of holoenzyme subunits. CaMKII is multifunctional; it targets a variety of cellular substrates, and this diversity depends on holoenzyme subunit composition. CaMKII comprises homooligomeric and heterooligomeric complexes generated from four subunits (α, β, δ, and γ) encoded by separate genes that are further expanded by extensive alternative splicing to more than 30 different isoforms. Much attention has been paid to understanding the regulation of CaMKII function through its structural diversity and/or substrate specificity. However, given the importance of subunit composition to holoenzyme activity, it is likely that specificity of cellular expression of CaMKII isoforms also plays a major role in regulation of enzyme function. Herein we review the cellular colocalization of CaMKII isoforms with special regard to the cell-type specificity of isoform expression in brain. In addition, we highlight the remarkable specificity of subcellular localization by the CaMKIIα isoform. In addition, we discuss the role that this cellular specificity of expression might play in propagating the type of recurrent neuronal activity associated with disorders such as temporal lobe epilepsy. Wiley Periodicals, Inc. © 2012 International League Against Epilepsy.
            Article 0 comments Cited 50 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Continuous peripheral nerve blocks in hospital wards after orthopedic surgery: a multicenter prospective analysis of the quality of postoperative analgesia and complications in 1,416 patients.

              Sophie Bringuier, Olivier Choquet, Philippe Pirat … (2005)
              Continuous peripheral nerve block (CPNB) is the technique of choice for postoperative analgesia after painful orthopedic surgery. However, the incidence of neurologic and infectious adverse events in the postoperative period are not well established. This issue was the aim of the study. Patients scheduled to undergo orthopedic surgery performed with a CPNB were prospectively included during 1 yr in a multicenter study. Efficacy of postoperative analgesia, bacteriologic cultures of the catheter, and acute neurologic and infectious adverse events were evaluated after surgery in 1,416 patients at arrival in the postanesthesia care unit, at hour 1, and every 24 h up to day 5. Risk factors for adverse events were determined using logistic regression. The median duration of CPNB was 56 h. Both general anesthesia and CPNB were performed in 73.6% of the patients. Postoperative analgesia was effective in 96.3%, but an increase in pain scores was noted at hour 24 (P = 0.01). Hypoesthesia or numbness occurred in 3% and 2.2%, respectively, and paresthesia occurred in 1.5%. Three neural lesions (0.21%) were noted after continuous femoral nerve block. Two of these patients were anesthetized during block procedure. Nerve damage completely resolved 36 h to 10 weeks later. Cultures from 28.7% of the catheters were positive. Three percent of patients had local inflammatory signs. The bacterial species most frequently found were coagulase-negative staphylococcus (61%) and gram-negative bacillus (21.6%). A Staphylococcus aureus psoas abscess (0.07%) was reported in one diabetic woman. Independent risk factors for paresthesia/dysesthesia were postoperative monitoring in intensive care, age less than 40 yr, and use of bupivacaine. Risk factors for local inflammation/infection were postoperative monitoring in intensive care, catheter duration greater than 48 h, male sex, and absence of antibiotic prophylaxis. CPNB is an effective technique for postoperative analgesia. Minor incidents and bacterial colonization of catheters are frequent, with no adverse clinical consequences in the large majority of cases. Major neurologic and infectious adverse events are rare.
              Article 0 comments Cited 41 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Xian-Jie Wen: xjwen166@163.com
                Heng Li: aheng@163.com
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 12 July 2017
                Publication date PMC-release: 12 July 2017
                Publication date Collection: 2017
                Volume: 7
                Electronic Location Identifier: 5262
                Affiliations
                [1 ]ISNI 0000 0004 0604 5998, GRID grid.452881.2, Department of Anesthesiology, , The First People’s Hospital of Foshan & Foshan Hospital of Sun Yat-sen University, ; Foshan, 528000 Guangdong Province China
                [2 ]Department of Anesthesiology, The sixth affiliated hospital of Guangzhou medical university, Qinyuan, 511518 Guangdong Province China
                Article
                Publisher ID: 5678
                DOI: 10.1038/s41598-017-05678-2
                PMC ID: 5507888
                PubMed ID: 28701796
                SO-VID: e93659ef-535f-4b77-95d6-c71c0a983f4a
                Copyright © © The Author(s) 2017
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 10 January 2017
                Date accepted : 1 June 2017
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2017

                ScienceOpen disciplines: Uncategorized
                Data availability:
                ScienceOpen disciplines: Uncategorized

                Comments

                Comment on this article

                scite_

                Similar content308

                See all similar

                Cited by1

                See all cited by

                Most referenced authors182

                See all reference authors