CaMKII

出典: meddic

calcium-calmodulin-dependent protein kinase type 2calmodulin kinase IIcalmodulin-dependent protein kinase II、CaM KII、CaM kinase II

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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2014/02/24 23:56:39」(JST)

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英文文献

  • AMPA receptor upregulation in the nucleus accumbens shell of cocaine-sensitized rats depends upon S-nitrosylation of stargazin.
  • Selvakumar B1, Campbell PW2, Milovanovic M2, Park DJ2, West AR2, Snyder SH3, Wolf ME4.Author information 1Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.2Department of Neuroscience, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.3Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Psychiatry, The Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: ssnyder@jhmi.edu.4Department of Neuroscience, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA. Electronic address: marina.wolf@rosalindfranklin.edu.AbstractBehavioral sensitization to cocaine is associated with increased AMPA receptor (AMPAR) surface expression in the nucleus accumbens (NAc). This upregulation is withdrawal-dependent, as it is not detected on withdrawal day (WD) 1, but is observed on WD7-21. Its underlying mechanisms have not been clearly established. Nitric oxide (NO) regulates AMPAR trafficking in the brain by S-nitrosylation of the AMPAR auxiliary subunit, stargazin, leading to increased AMPAR surface expression. Our goal was to determine if stargazin S-nitrosylation contributes to AMPAR upregulation during sensitization. First, we measured stargazin S-nitrosylation in NAc core and shell subregions on WD14 after 8 daily injections of saline or 15 mg/kg cocaine. Stargazin S-nitrosylation was markedly increased in NAc shell but not core. To determine if this is associated with AMPAR upregulation, rats received 8 cocaine or saline injections followed by twice-daily treatments with vehicle or the nitric oxide synthase inhibitor l-NAME (50 mg/kg) on WD1-6, the time when AMPAR upregulation is developing in cocaine-exposed rats. Cocaine/vehicle rats showed elevated stargazin and GluA1 surface expression on WD7 compared to saline/vehicle rats; the GluA1 increase was more robust in core, while stargazin increased more robustly in shell. These effects of cocaine were attenuated in shell but not core when cocaine injections were followed by l-NAME treatment on WD1-6. Together, these results indicate that elevated S-nitrosylation of stargazin contributes to AMPAR upregulation during sensitization selectively in the NAc shell. It is possible that AMPAR upregulation in core involves a different TARP, γ4, which also upregulates in the NAc of sensitized rats.
  • Neuropharmacology.Neuropharmacology.2014 Feb;77:28-38. doi: 10.1016/j.neuropharm.2013.08.036. Epub 2013 Sep 10.
  • Behavioral sensitization to cocaine is associated with increased AMPA receptor (AMPAR) surface expression in the nucleus accumbens (NAc). This upregulation is withdrawal-dependent, as it is not detected on withdrawal day (WD) 1, but is observed on WD7-21. Its underlying mechanisms have not been clea
  • PMID 24035918
  • The effects of intraganglionic injection of calcium/calmodulin-dependent protein kinase II inhibitors on pain-related behavior in diabetic neuropathy.
  • Jelicic Kadic A1, Boric M2, Kostic S3, Sapunar D4, Puljak L5.Author information 1Laboratory for Pain Research, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia. Electronic address: antonia.jelicic@mefst.hr.2Laboratory for Pain Research, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia. Electronic address: matija.boric.st@gmail.com.3Laboratory for Pain Research, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia. Electronic address: sandra.kostic@mefst.hr.4Laboratory for Pain Research, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia. Electronic address: ds@mefst.hr.5Laboratory for Pain Research, University of Split School of Medicine, Soltanska 2, 21000 Split, Croatia. Electronic address: livia@mefst.hr.AbstractCalcium/calmodulin-dependent protein kinase II (CaMKII) has been implicated in the transmission of nociceptive input in diabetic neuropathy. The aim of this study was to test whether intraganglionic (i.g.) injection of CaMKII inhibitors may alleviate pain-related behavior in diabetic rats. Diabetes was induced in Sprague-Dawley rats using 55mg/kg streptozotocin intraperitoneally. Two weeks after diabetes induction, CaMKII inhibitors myristoil-AIP and KN93 were injected directly into the right L5 dorsal root ganglion (DRG). Behavioral testing with mechanical and thermal stimuli was performed before induction of diabetes, the day preceding the injection, as well as 2 and 24h after the i.g. injection. The expression of total CaMKII and its alpha isoform in DRG neurons was analyzed using immunohistochemistry. CaMKII inhibitors attenuated pain-related behavior in a modality-specific fashion. Attenuation of nociceptive behavior was accompanied with a corresponding decrease of CaMKII alpha expression in DRG neurons on the side of injection. A significant decrease of CaMKII alpha expression was seen in small- and medium-sized neurons. In conclusion, our study provides evidence that CaMKII inhibitors are potential pharmacological agents that should be further explored for treatment of diabetic neuropathy symptoms.
  • Neuroscience.Neuroscience.2014 Jan 3;256:302-8. doi: 10.1016/j.neuroscience.2013.10.032. Epub 2013 Oct 23.
  • Calcium/calmodulin-dependent protein kinase II (CaMKII) has been implicated in the transmission of nociceptive input in diabetic neuropathy. The aim of this study was to test whether intraganglionic (i.g.) injection of CaMKII inhibitors may alleviate pain-related behavior in diabetic rats. Diabetes
  • PMID 24161721
  • Tripchlorolide improves age-associated cognitive deficits by reversing hippocampal synaptic plasticity impairment and NMDA receptor dysfunction in SAMP8 mice.
  • Lin N, Pan XD, Chen AQ, Zhu YG, Wu M, Zhang J, Chen XC.Author information Department of Neurology, Fujian Institute of Geriatrics, Fujian Medical University Union Hospital, 29 Xinquan Road, Fuzhou 350001, China; Key Laboratory of Brain Aging and Neurodegenerative Disease, Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, 29 Xinquan Road, Fuzhou 350001, China.AbstractDeficits in cognition and performance accompanying age-related neurodegenerative diseases such as Alzheimer's disease (AD) are closely associated with the impairment of synaptic plasticity. Here, using a mouse model of senescence-accelerated P8 (SAMP8), we reported the role of tripchlorolide (T4), an extract of the natural herb Tripterygium wilfordii Hook F, in improving cognitive deficits and promoting the long-term potentiation (LTP) of hippocampal slices via the N-methyl-d-aspartate receptor (NMDAR)-dependent signaling pathway. Our results demonstrated that chronic administration of T4 at low doses (0.25, 1.0, or 4.0μg/kg per day, injected intraperitoneally for 75 days) significantly improved learning and memory function in aged SAMP8 mice, as indicated by a chain of behavioral tests including the Y-maze and Morris water maze. Additionally, T4 reversed the impaired LTP in hippocampal CA1 regions of SAMP8 mice in a dose-dependent manner. Moreover, it upregulated the levels of phospho-NMDAR1, postsynaptic density-95 (PSD-95), phospho-calcium-calmodulin dependent kinase II (CaMKII), phospho-CREB and brain derived neurotrophic factor (BDNF) in the hippocampus. This indicates that T4 prevents the impairment of NMDAR-mediated synaptic plasticity-related signal molecules. At optimal doses, T4 did not show significant side-effects on blood counts, blood biochemical measures, or survival of the mice. This novel mechanism in reversing age-related synaptic dysfunction and NMDAR functional deficits suggests that T4 can halt the manifestation of a key early-stage event in AD. With the consideration of SAMP8 mice as a model to develop therapeutic interventions for AD, our findings provide new insight into the clinical application of tripchlorolide in AD treatment.
  • Behavioural brain research.Behav Brain Res.2014 Jan 1;258:8-18. doi: 10.1016/j.bbr.2013.10.010. Epub 2013 Oct 17.
  • Deficits in cognition and performance accompanying age-related neurodegenerative diseases such as Alzheimer's disease (AD) are closely associated with the impairment of synaptic plasticity. Here, using a mouse model of senescence-accelerated P8 (SAMP8), we reported the role of tripchlorolide (T4), a
  • PMID 24140565

和文文献

  • Anti-hyperalgesic effect of CaMKII inhibitor is associated with downregulation of phosphorylated CREB in rat spinal cord
  • WANG Yanxia,CHENG Xinzhi,XU Jing,LIU Zhe,WAN Yanjie,MA Daqing
  • Journal of anesthesia 25(1), 87-92, 2011-02-20
  • NAID 10029021929
  • Pharmacological Study on Alzheimer’s Drugs Targeting Calcium/Calmodulin-Dependent Protein Kinase II
  • Moriguchi Shigeki
  • Journal of Pharmacological Sciences 117(1), 6-11, 2011
  • … Furthermore, nefiracetam-induced LTP enhancement was closely associated with calcium/calmodulin-dependent protein kinase II (CaMKII) activation with concomitant increase in phosphorylation of AMPA-type glutamate receptor subunit 1 (GluA1) (Ser-831) as a postsynaptic CaMKII substrate. … In conclusion, nefiracetam enhances NMDA-receptor function through stimulation of its glycine binding site and nefiracetam-induced CaMKII activation likely contributes to improvement of cognition, learning, and memory. …
  • NAID 130001011760

関連リンク

図1:CaMKIIの活性制御機構通常の神経活動状態では、細胞内のCa2+/ カルモジュリン(Ca2+/CaM)濃度、CaMKII自身の活性、脱リン酸化酵素である フォスファターゼ(phosphatases)活性のバランスによって、CaMKIIの活性状態は平衡 状態に保たれてい ...
Calcium/calmodulin-dependent protein kinase II (CaMKII) is an enzyme that accounts for 1-2% of all of the proteins in the brain. This kinase can exist as 28 different isoforms. The isoforms of CaMKII derive from the alpha, beta, gamma, and ...

関連画像

CaMKII RegulationFile:CaMKII-dodecameric.pngClick on image to view larger version.camkiiFile:CaMKII.pngCamkii


★リンクテーブル★
リンク元CaM kinase II」「カルモジュリン依存性プロテインキナーゼII」「カルモジュリンキナーゼII」「calmodulin kinase II」「calmodulin-dependent protein kinase II
関連記事CaMKI」「CaMK

CaM kinase II」

  [★]

calcium-calmodulin-dependent protein kinase type 2calmodulin kinase IIcalmodulin-dependent protein kinase II、CaM KII、CaMKII


カルモジュリン依存性プロテインキナーゼII」

  [★]

calmodulin-dependent protein kinase IIcalmodulin kinase IICaM kinase IICaMKII
カルシウム・カルモジュリン依存性プロテインキナーゼ2型CaMキナーゼIIカルモジュリンキナーゼIIカルモジュリン依存性キナーゼII


カルモジュリンキナーゼII」

  [★]

calmodulin kinase IICaM kinase IICaMKII、CaM KII
カルシウム・カルモジュリン依存性プロテインキナーゼ2型CaMキナーゼIIカルモジュリン依存性プロテインキナーゼIIカルモジュリン依存性キナーゼII


calmodulin kinase II」

  [★]

calmodulin-dependent protein kinase II、CaM KII、CaM kinase IICaMKII


calmodulin-dependent protein kinase II」

  [★]

calcium-calmodulin-dependent protein kinase type 2calmodulin kinase II、CaM KII、CaM kinase IICaMKII


CaMKI」

  [★]

calmodulin kinase Icalmodulin-dependent protein kinase I、CaM KI、CaM kinase I


CaMK」

  [★]

カルモジュリンキナーゼカルモジュリン依存性プロテインキナーゼ

calmodulin kinasecalmodulin-dependent protein kinaseCaM kinase


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