Differential expression of phosphorylated Ca2+/calmodulin-dependent protein kinase II and phosphorylated extracellular signal-regulated protein in the mouse hippocampus induced by various nociceptive stimuli

Seo, Young-Jun; Kwon, Min-Soo; Choi, Ho-Kyew; Choi, Seong-Soo; Kim, Y.-W.; Lee, J.-K.; Park, S.-H.; Jung, Jun‐Sub; Suh, Hong‐Won

doi:10.1016/j.neuroscience.2008.08.002

Cited by 13 publications

(11 citation statements)

References 59 publications

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“…In a mouse model of pain induced by subcutaneous injection of formalin, Seo et al [45] reported that intrathecal and intraperitoneal injection of glutamate or acetic acid resulted in up-regulation of hippocampal phosphorylated Ca 2+ /calmodulin-dependent protein kinase II alpha or phosphorylated extracellular signal-regulated protein expression. In repeated stress stimulation-induced depression rats, EA also increased the number of p-CREB-positive neurons in the hippocampus and restored hippocampal BDNF mRNA expression induced by immobilization stress [46].…”

Section: Discussionmentioning

confidence: 99%

Differential proteomics analysis of the analgesic effect of electroacupuncture intervention in the hippocampus following neuropathic pain in rats

Gao

Chen

Wang

et al. 2012

BMC Complement Altern Med

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BackgroundEvidence is building steadily on the effectiveness of acupuncture therapy in pain relief and repeated acupuncture-induced pain relief is accompanied by improvement of hippocampal neural synaptic plasticity. To further test the cellular and molecular changes underlying analgesic effect of acupuncture, the global change of acupuncture associated protein profiles in the hippocampus under neuropathic pain condition was profiled.MethodsThe chronic constrictive injury (CCI) model was established by ligature of the unilateral sciatic nerve in adult Wistar rats. Rats were randomized into normal control (NC) group, CCI group, and CCI with electroacupuncture (EA) stimulation group. EA was applied to bilateral Zusanli (ST36) and Yanglingquan (GB34) in the EA group. Differentially expressed proteins in the hippocampus in the three groups were identified by two-dimensional gel electrophoresis and matrix-assisted laser desorption/ionization time of flight mass spectrometry. The functional clustering of the identified proteins was analyzed by Mascot software.ResultsAfter CCI, the thermal pain threshold of the affected hind footpad was decreased and was reversed gradually by 12 sessions of acupuncture treatment. Following EA, there were 19 hippocampal proteins identified with significant changes in expression (>2-fold), which are involved in metabolic, physiological, and cellular processes. The top three canonical pathways identified were “cysteine metabolism”, “valine, leucine, and isoleucine degradation” and “mitogen-activated protein kinase (MAPK) signaling”.ConclusionsThese data suggest that the analgesic effect of EA is mediated by regulation of hippocampal proteins related to amino acid metabolism and activation of the MAPK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Differential proteomics analysis of the analgesic effect of electroacupuncture intervention in the hippocampus following neuropathic pain in rats

Gao

Chen

Wang

et al. 2012

BMC Complement Altern Med

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“…Control saline and drug solutions were freshly prepared under sterile conditions immediately before each use. The selection of this drug was based on its selective inhibitory effect on intracellular CaMKII activation (Tokumitsu et al, 1990; Ogawa et al, 2005; Seo et al, 2008; Shioda et al, 2011). Commercially available KN-93 is suitable for microinjection studies because it is water soluble, cell-permeable, and has reversible effects.…”

Section: Methodsmentioning

confidence: 99%

“…Commercially available KN-93 is suitable for microinjection studies because it is water soluble, cell-permeable, and has reversible effects. It has also been used successfully in past microinjection studies in behaving animals (Pierce et al, 1998; Fleegal and Sumners, 2003; Licata et al, 2004; Ogawa et al, 2005; Sakurai et al, 2007; Loweth et al, 2008; Seo et al, 2008; Myskiw et al, 2010; Ota et al, 2010; Shioda et al, 2011). …”

Section: Methodsmentioning

confidence: 99%

Calcium/Calmodulin Kinase II in the Pedunculopontine Tegmental Nucleus Modulates the Initiation and Maintenance of Wakefulness

Datta¹,

O’Malley²,

Patterson³

2011

J. Neurosci.

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The pedunculopontine tegmentum nucleus (PPT) is critically involved in the regulation of wakefulness (W) and rapid eye movement (REM) sleep, but our understanding of the mechanisms of this regulation remains incomplete. The present study was designed to determine the role of PPT intracellular calcium/calmodulin kinase (CaMKII) signaling in the regulation of W and sleep. To achieve this aim, three different concentrations (0.5, 1.0, and 2.0 nmol) of the CaMKII activation inhibitor, KN-93, were microinjected bilaterally (100 nl/site) into the PPT of freely moving rats, and the effects on W, slow-wave sleep (SWS), REM sleep, and levels of phosphorylated CaMKII (pCaMKII) expression in the PPT were quantified. These effects, which were concentration-dependent and affected wake–sleep variables for 3 h, resulted in decreased W, due to reductions in the number and duration of W episodes; increased SWS and REM sleep, due to increases in episode duration; and decreased levels of pCaMKII expression in the PPT. Regression analyses revealed that PPT levels of pCaMKII were positively related with the total percentage of time spentin W (R2 = 0.864; n = 28 rats; p < 0.001) and negatively related with the total percentage of time spentin sleep (R2 = 0.863; p < 0.001). These data provide the first direct evidence that activation of intracellular CaMKII signaling in the PPT promotes W and suppresses sleep. These findings are relevant for designing a drug that could treat excessive sleepiness by promoting alertness.

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“…In another study, Liang et al (2004b) demonstrated that the expression of spinal CaMKIIa was almost unchanged after hindpaw formalin injection in heme oxygenase type 2 (HO-2)-null mutant mice, indicating that CaMKII activity is modulated by HO-2. Increased CaMKII activity was also found in the mouse hippocampus after subcutaneous injection of formalin and intracerebroventricular injection of KN-93 alleviated formalin-induced pain behaviors (Seo et al, 2008). Moreover, our previous study also examined the analgesic effect of CaMKII inhibitors on CFA-induced inflammatory pain (Luo et al, 2008).…”

Section: Camkii and Inflammatory Painmentioning

confidence: 88%

Cellular and Molecular Mechanisms of Calcium/Calmodulin-Dependent Protein Kinase II in Chronic Pain

Zhou

Liu

Chen

et al. 2017

J Pharmacol Exp Ther

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Chronic pain, often defined as any pain lasting more than 3 months, is poorly managed because of its multifaceted and complex mechanisms. Calcium/calmodulin-dependent protein kinase II (CaMKII) is a multifunctional serine/threonine kinase that plays a fundamental role in synaptic plasticity, learning, and memory. Recent emerging evidence demonstrates increased expression and activity of CaMKII in the spinal cord and dorsal root ganglia of various chronic pain models. Moreover, our previous studies also find that inhibiting CaMKII could attenuate inflammatory pain and neuropathic pain. In this review, we provide evidence for the involvement of CaMKII in the initiation and development of chronic pain, including neuropathic pain, bone cancer pain, and inflammatory pain. Novel CaMKII inhibitors with potent inhibitory effect and high specificity may be alternative therapeutic strategies for the management of chronic pain in the future.

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Differential expression of phosphorylated Ca2+/calmodulin-dependent protein kinase II and phosphorylated extracellular signal-regulated protein in the mouse hippocampus induced by various nociceptive stimuli

Cited by 13 publications

References 59 publications

Differential proteomics analysis of the analgesic effect of electroacupuncture intervention in the hippocampus following neuropathic pain in rats

Differential proteomics analysis of the analgesic effect of electroacupuncture intervention in the hippocampus following neuropathic pain in rats

Calcium/Calmodulin Kinase II in the Pedunculopontine Tegmental Nucleus Modulates the Initiation and Maintenance of Wakefulness

Cellular and Molecular Mechanisms of Calcium/Calmodulin-Dependent Protein Kinase II in Chronic Pain

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