Neurosignals最新文献_第8页

Modulation of action potential trains in rabbit saphenous nerve unmyelinated fibers. 兔隐神经无髓纤维动作电位序列的调节。

Neurosignals Pub Date : 2013-01-01 Epub Date: 2012-08-01 DOI: 10.1159/000337350

Zhi-Ru Zhu, Yi-Hui Liu, Wei-Gang Ji, Jian-Hong Duan, San-Jue Hu

{"title":"Modulation of action potential trains in rabbit saphenous nerve unmyelinated fibers.","authors":"Zhi-Ru Zhu, Yi-Hui Liu, Wei-Gang Ji, Jian-Hong Duan, San-Jue Hu","doi":"10.1159/000337350","DOIUrl":"https://doi.org/10.1159/000337350","url":null,"abstract":"Usually, the main axon is assumed to faithfully conduct action potentials (APs). Recent data have indicated that neural processing can occur along the axonal path. However, the patterns and mechanisms of temporal coding are not clear. In the present study, single fiber recording was used to analyze activity-dependent modulation of AP trains in the main axons of C fibers in the rabbit saphenous nerve. Trains of 5 superthreshold electrical pulses at interstimulus intervals of 20 or 50 ms were applied to the nerve trunk for 200 s. The interspike intervals (ISIs) for these trains were compared to the input interstimulus intervals. Three basic types of C fibers were observed in response to repeated stimuli: first, the ISI between the first and second AP (ISI1-2) of type 1 was longer than the interstimulus interval; second, the ISI1-2 of type 2 showed wavelike fluctuations around the interstimulus interval, and third, the ISI1-2 of type 3 exhibited shorter intervals for a long period. Furthermore, both 4-aminopyridine-sensitive potassium and hyperpolarization-activated cation currents were involved in the modulation of ISI1-2 of train pulses. These data provide new evidence that multiple modes of neural conduction can occur along the main axons of C fibers.","PeriodicalId":19171,"journal":{"name":"Neurosignals","volume":"21 3-4","pages":"213-28"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000337350","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30816217","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Contribution of SDF-1α/CXCR4 signaling to brain development and glioma progression. SDF-1α/CXCR4信号在脑发育和胶质瘤进展中的作用

Neurosignals Pub Date : 2013-01-01 Epub Date: 2012-08-21 DOI: 10.1159/000339091

Zheng Jiang, Wei Zhou, Shanghui Guan, Jianbo Wang, Yemin Liang

引用次数: 29

Anorexigenic and orexigenic hormone modulation of mammalian target of rapamycin complex 1 activity and the regulation of hypothalamic agouti-related protein mRNA expression. 厌食和促食欲激素对哺乳动物雷帕霉素靶复合物 1 活性的调节和下丘脑激动相关蛋白 mRNA 表达的调控。

Neurosignals Pub Date : 2013-01-01 Epub Date: 2012-03-28 DOI: 10.1159/000334144

Kenneth R Watterson, Dawn Bestow, Jennifer Gallagher, D Lee Hamilton, Fiona B Ashford, Paul J Meakin, Michael L J Ashford

{"title":"Anorexigenic and orexigenic hormone modulation of mammalian target of rapamycin complex 1 activity and the regulation of hypothalamic agouti-related protein mRNA expression.","authors":"Kenneth R Watterson, Dawn Bestow, Jennifer Gallagher, D Lee Hamilton, Fiona B Ashford, Paul J Meakin, Michael L J Ashford","doi":"10.1159/000334144","DOIUrl":"10.1159/000334144","url":null,"abstract":"Activation of mammalian target of rapamycin 1 (mTORC1) by nutrients, insulin and leptin leads to appetite suppression (anorexia). Contrastingly, increased AMP-activated protein kinase (AMPK) activity by ghrelin promotes appetite (orexia). However, the interplay between these mechanisms remains poorly defined. The relationship between the anorexigenic hormones, insulin and leptin, and the orexigenic hormone, ghrelin, on mTORC1 signalling was examined using S6 kinase phosphorylation as a marker for changes in mTORC1 activity in mouse hypothalamic GT1-7 cells. Additionally, the contribution of AMPK and mTORC1 signalling in relation to insulin-, leptin- and ghrelin-driven alterations to mouse hypothalamic agouti-related protein (AgRP) mRNA levels was examined. Insulin and leptin increase mTORC1 activity in a phosphoinositide-3-kinase (PI3K)- and protein kinase B (PKB)-dependent manner, compared to vehicle controls, whereas increasing AMPK activity inhibits mTORC1 activity and blocks the actions of the anorexigenic hormones. Ghrelin mediates an AMPK-dependent decrease in mTORC1 activity and increases hypothalamic AgRP mRNA levels, the latter effect being prevented by insulin in an mTORC1-dependent manner. In conclusion, mTORC1 acts as an integration node in hypothalamic neurons for hormone-derived PI3K and AMPK signalling and mediates at least part of the assimilated output of anorexigenic and orexigenic hormone actions in the hypothalamus.","PeriodicalId":19171,"journal":{"name":"Neurosignals","volume":"21 1-2","pages":"28-41"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ba/e7/nsg-0021-0028.PMC3704126.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30535758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Stroke increases g protein-coupled estrogen receptor expression in the brain of male but not female mice. 中风增加了雄性小鼠大脑中g蛋白偶联雌激素受体的表达，而雌性小鼠没有。

Neurosignals Pub Date : 2013-01-01 Epub Date: 2012-08-01 DOI: 10.1159/000338019

Brad R S Broughton, Vanessa H Brait, Elizabeth Guida, Seyoung Lee, Thiruma V Arumugam, Chantelle V Gardiner-Mann, Alyson A Miller, Sung-Chun Tang, Grant R Drummond, Christopher G Sobey

{"title":"Stroke increases g protein-coupled estrogen receptor expression in the brain of male but not female mice.","authors":"Brad R S Broughton, Vanessa H Brait, Elizabeth Guida, Seyoung Lee, Thiruma V Arumugam, Chantelle V Gardiner-Mann, Alyson A Miller, Sung-Chun Tang, Grant R Drummond, Christopher G Sobey","doi":"10.1159/000338019","DOIUrl":"https://doi.org/10.1159/000338019","url":null,"abstract":"The novel estrogen receptor, G protein-coupled estrogen receptor (GPER, previously named GPR30), is widely distributed throughout the male and female brain and, thus, could potentially play a role in estrogen-mediated neuroprotective effects in diseases such as stroke. We hypothesized that GPER distribution and expression in the brain of male, intact female, and ovariectomized (OVX) mice is increased after 0.5 h middle cerebral artery occlusion. Using immunohistochemistry, we found that ischemia reperfusion increased GPER distribution in the peri-infarct brain regions of male mice, but surprisingly not in intact females or OVX mice. Similar differences were observed in the male and female human brain after stroke. In contrast, GPER distribution was decreased in the infarct core of all mice examined. Furthermore, GPER immunofluorescence was co-localized with the endothelial cell marker, von Willebrand factor, and the neuronal marker, NeuN. Consistent with the immunohistochemical findings, Western blot analysis showed GPER expression is only elevated in the ischemic hemisphere of male mice. Moreover, GPER mRNA expression in males was elevated at 4 h but had returned to baseline by 24 h. In conclusion, these findings indicate that GPER may be a potential therapeutic target after stroke, especially in males, in whom estrogen therapy is not feasible.","PeriodicalId":19171,"journal":{"name":"Neurosignals","volume":"21 3-4","pages":"229-39"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000338019","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30816455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 53

Differential contribution of the guanylyl cyclase-cyclic GMP-protein kinase G pathway to the proliferation of neural stem cells stimulated by nitric oxide. 关酰环化酶-环gmp -蛋白激酶G通路对一氧化氮刺激神经干细胞增殖的差异贡献。

Neurosignals Pub Date : 2013-01-01 Epub Date: 2012-02-23 DOI: 10.1159/000332811

Bruno P Carreira, Maria Inês Morte, Ana Sofia Lourenço, Ana Isabel Santos, Angela Inácio, António F Ambrósio, Caetana M Carvalho, Inês M Araújo

{"title":"Differential contribution of the guanylyl cyclase-cyclic GMP-protein kinase G pathway to the proliferation of neural stem cells stimulated by nitric oxide.","authors":"Bruno P Carreira, Maria Inês Morte, Ana Sofia Lourenço, Ana Isabel Santos, Angela Inácio, António F Ambrósio, Caetana M Carvalho, Inês M Araújo","doi":"10.1159/000332811","DOIUrl":"https://doi.org/10.1159/000332811","url":null,"abstract":"Nitric oxide (NO) is an important inflammatory mediator involved in the initial boost in the proliferation of neural stem cells following brain injury. However, the mechanisms underlying the proliferative effect of NO are still unclear. The aim of this work was to investigate whether cyclic GMP (cGMP) and the cGMP-dependent kinase (PKG) are involved in the proliferative effect triggered by NO in neural stem cells. For this purpose, cultures of neural stem cells isolated from the mouse subventricular zone (SVZ) were used. We observed that long-term exposure to the NO donor (24 h), NOC-18, increased the proliferation of SVZ cells in a cGMP-dependent manner, since the guanylate cyclase inhibitor, ODQ, prevented cell proliferation. Similarly to NOC-18, the cGMP analogue, 8-Br-cGMP, also increased cell proliferation. Interestingly, shorter exposures to NO (6 h) increased cell proliferation in a cGMP-independent manner via the ERK/MAP kinase pathway. The selective inhibitor of PKG, KT5823, prevented the proliferative effect induced by NO at 24 h but not at 6 h. In conclusion, the proliferative effect of NO is initially mediated by the ERK/MAPK pathway, and at later stages by the GC/cGMP/PKG pathway. Thus, our work shows that NO induces neural stem cell proliferation by targeting these two pathways in a biphasic manner.","PeriodicalId":19171,"journal":{"name":"Neurosignals","volume":"21 1-2","pages":"1-13"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000332811","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30495918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 24

Coincidence signaling of dopamine D1-like and M1 muscarinic receptors in the regulation of cyclic AMP formation and CREB phosphorylation in mouse prefrontal cortex. 多巴胺d1样受体和M1毒蕈碱受体在小鼠前额皮质环AMP形成和CREB磷酸化调控中的重合信号。

Neurosignals Pub Date : 2013-01-01 Epub Date: 2012-03-28 DOI: 10.1159/000335208

Maria C Olianas, Simona Dedoni, Pierluigi Onali

{"title":"Coincidence signaling of dopamine D1-like and M1 muscarinic receptors in the regulation of cyclic AMP formation and CREB phosphorylation in mouse prefrontal cortex.","authors":"Maria C Olianas, Simona Dedoni, Pierluigi Onali","doi":"10.1159/000335208","DOIUrl":"https://doi.org/10.1159/000335208","url":null,"abstract":"In the prefrontal cortex, dopamine D1-like and M1 muscarinic receptors are both involved in the regulation of attentional, cognitive and emotional processes but so far no information has been provided on their functional interaction. In the present study we show that in mouse medial prefrontal cortex, concomitant activation of M1 muscarinic receptors potentiated D1-like receptor-induced cyclic AMP formation through a mechanism involving activation of Gq/11 and the release of G protein βγ subunits. Immunohistochemical studies indicated that the adenylyl cyclase isoforms AC2 and AC4 are expressed in mouse prefrontal cortex and that they colocalize with D1-like receptors with a greater association for AC4. In primary cultures of frontal cortex neurons, D1-like receptor-induced Ser133 phosphorylation of the transcription factor cyclic AMP-responsive element binding protein (CREB) was potentiated by concurrent stimulation of M1 receptors. Suppression of AC4 expression with small interfering RNA transfection reduced D1 stimulation of cyclic AMP formation and CREB phosphorylation and abolished the M1 potentiation, whereas knockdown of AC2 had no significant effects. These data indicate that in mouse prefrontal cortex Gq/11-coupled M1 receptor and Gs-coupled D1-like receptor inputs converge on AC4 with a consequent enhancement of cyclic AMP formation and signaling to the nucleus.","PeriodicalId":19171,"journal":{"name":"Neurosignals","volume":"21 1-2","pages":"61-74"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000335208","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30536753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Endoplasmic reticulum stress and neurodegeneration in experimental cerebral malaria. 实验性脑疟疾的内质网应激和神经退行性变。

Neurosignals Pub Date : 2013-01-01 Epub Date: 2012-05-15 DOI: 10.1159/000336970

Sripada Santosh Anand, Phanithi Prakash Babu

{"title":"Endoplasmic reticulum stress and neurodegeneration in experimental cerebral malaria.","authors":"Sripada Santosh Anand, Phanithi Prakash Babu","doi":"10.1159/000336970","DOIUrl":"https://doi.org/10.1159/000336970","url":null,"abstract":"Experimental cerebral malaria (ECM) resulting from Plasmodium berghei ANKA (PbA) infection in mice results in neuronal cell death. However, the precise mechanisms leading to neuronal cell death in ECM have not been fully elucidated. In the present study, we report the presence of endoplasmic reticulum (ER) stress markers and activation of the unfolded protein response (UPR) in the brain during the pathogenesis of ECM. Specific findings included activation of PKR-like ERkinase, inositol-requiring enzyme 1 and cleavage of activating transcription factor (ATF) 6 indicating the activation of all three major arms of the UPR. Further, we found changes in the protein levels of phosphorylated eukaryotic initiation factor α (p-eIF2α), ATF4, growth arrest and DNA damage-inducible protein 34, B cell lymphoma protein 2 (BCL-2), BCL-2-associated X protein, caspase-7, cleavage of caspase-3, and caspase-12. Our results demonstrate that ER stress-induced neuronal cell death in PbA-infected mice is associated with the expression of the pro-apoptotic molecule CHOP and downregulation of anti-apoptotic ER quality control molecules binding immunoglobulin protein, calreticulin and calnexin. Further CHOP was found to be localized in neurons and plays an essential role in neuronal cell death as revealed by our Fluoro-Jade B double staining. These results implicate an imbalance between ER stress-mediated pro-apoptotic and anti-apoptotic/survival signalling as a critical determinant of neuronal cell death in ECM.","PeriodicalId":19171,"journal":{"name":"Neurosignals","volume":"21 1-2","pages":"99-111"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000336970","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30615897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 17

Dopamine inhibits high-frequency stimulation-induced long-term potentiation of intrinsic excitability in CA1 hippocampal pyramidal neurons. 多巴胺抑制高频刺激诱导的CA1海马锥体神经元内在兴奋性的长期增强。

Neurosignals Pub Date : 2013-01-01 Epub Date: 2012-09-27 DOI: 10.1159/000342435

Chun-ling Wei, Yi-hui Liu, Ming-hao Yang, Zhi-qiang Liu, Wei Ren

{"title":"Dopamine inhibits high-frequency stimulation-induced long-term potentiation of intrinsic excitability in CA1 hippocampal pyramidal neurons.","authors":"Chun-ling Wei, Yi-hui Liu, Ming-hao Yang, Zhi-qiang Liu, Wei Ren","doi":"10.1159/000342435","DOIUrl":"https://doi.org/10.1159/000342435","url":null,"abstract":"The efficiency of neural circuits is modified by changes not only in synaptic strength, but also in intrinsic excitability of neurons. In CA1 hippocampal pyramidal neurons, bidirectional changes in the intrinsic excitability are often presented after induction of synaptic long-term potentiation or depression. This plasticity of intrinsic excitability has been identified as a cellular correlate of learning. Besides, behavioral learning often involves action of reinforcement or rewarding mediated by dopamine (DA). Here, we examined how DA influences the intrinsic plasticity of CA1 hippocampal pyramidal neurons when high-frequency stimulation (HFS) was applied to Schaffer collaterals. The results showed that DA inhibits the decrease in rheobase and increase in mean firing rate of pyramidal neurons induced by HFS, and that this inhibition was abolished by the D1-like receptor antagonist SCH23390 but not by the D2-like receptor antagonist sulpiride. The results suggest that DA inhibits the potentiation of excitability induced by presynaptic HFS, and that this inhibition depends on the activation of D1-like receptors.","PeriodicalId":19171,"journal":{"name":"Neurosignals","volume":"21 3-4","pages":"150-9"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000342435","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30939995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Brain-site-specific proteome changes induced by neuronal P60TRP expression. 神经元P60TRP表达诱导的脑位点特异性蛋白质组变化。

Neurosignals Pub Date : 2013-01-01 Epub Date: 2013-02-06 DOI: 10.1159/000343672

Arulmani Manavalan, Manisha Mishra, Siu Kwan Sze, Klaus Heese

{"title":"Brain-site-specific proteome changes induced by neuronal P60TRP expression.","authors":"Arulmani Manavalan, Manisha Mishra, Siu Kwan Sze, Klaus Heese","doi":"10.1159/000343672","DOIUrl":"https://doi.org/10.1159/000343672","url":null,"abstract":"p60 transcription regulator protein (p60TRP) facilitates the processing of the amyloid precursor protein towards the non-amyloidogenic pathway by inhibiting the β-secretase action. This protein was initially identified to be downregulated in the temporal lobe of brains from Alzheimer's disease patients. p60TRP is one of the G-protein-coupled receptor (GPCR)-associated proteins which directly influences the signalling capacity of GPCRs. In the present study, we investigated the brain-region-specific proteome profile of transgenic p60TRP mice to gain an insight into the molecular events mediated by the long-term effect of neuronal p60TRP overexpression on brain proteome changes and its potential implication for neuronal functions in the central nervous system. Using a proteomics research approach based on isobaric tags for relative and absolute quantitation, we identified 2,025 proteins, whereby 1,735 proteins were quantified, out of which 56 were found to be significantly altered in the cortex and/or hippocampus of neuronal transgenic neuronal p60TRP mice. Our data suggests that in vivo overexpression of neuronal p60TRP significantly affects cognitive and neuroprotective capacities.","PeriodicalId":19171,"journal":{"name":"Neurosignals","volume":"21 3-4","pages":"129-49"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000343672","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31223418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 19

Cdk5 phosphorylates a component of the HDAC complex and regulates histone acetylation during neuronal cell death. Cdk5磷酸化HDAC复合物的一个组分，并在神经元细胞死亡过程中调节组蛋白乙酰化。

Neurosignals Pub Date : 2013-01-01 Epub Date: 2012-03-06 DOI: 10.1159/000335158

Amy K Y Fu, Kwok-Wang Hung, Hovy Ho-Wai Wong, Wing-Yu Fu, Nancy Y Ip

{"title":"Cdk5 phosphorylates a component of the HDAC complex and regulates histone acetylation during neuronal cell death.","authors":"Amy K Y Fu, Kwok-Wang Hung, Hovy Ho-Wai Wong, Wing-Yu Fu, Nancy Y Ip","doi":"10.1159/000335158","DOIUrl":"https://doi.org/10.1159/000335158","url":null,"abstract":"Cyclin-dependent kinase 5 (Cdk5), a member of the cyclin-dependent kinase family, is critical for regulating neural development and neuronal survival. Dysregulation of Cdk5 is associated with abnormal expression of cell cycle-related proteins during neuronal apoptosis. We have previously found that p35, a Cdk5 activator, interacts with mSds3, an integral component of the histone deacetylase complex in vitro, suggesting a functional role of Cdk5 in gene regulation through modulation of chromatin integrity. In this study, we further demonstrate that Cdk5-dependent phosphorylation of mSds3 at Ser228 occurs in mouse brain nuclei. The expression of mSds3 protein and its interaction with Cdk5 activators is developmentally regulated in the mouse brain. Importantly, our findings suggest that the ability of Cdk5 to regulate activity deprivation-induced apoptosis of cerebellar granule neurons is likely mediated by the regulation of histone acetylation. Suppression of Cdk5 not only attenuates the induction of histone H3 acetylation and the aberrant upregulation of cyclin proteins in neurons after activity deprivation, but also results in protection of neurons against apoptotic cell death. Taken together, our findings suggest that Cdk5 regulates neuronal survival by precise epigenetic control through modulation of histone acetylation.","PeriodicalId":19171,"journal":{"name":"Neurosignals","volume":" ","pages":"55-60"},"PeriodicalIF":0.0,"publicationDate":"2013-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000335158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40145193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 12