Neuron glia biology最新文献

Trigeminal satellite cells modulate neuronal responses to triptans: relevance for migraine therapy. 三叉神经卫星细胞调节对曲坦类药物的神经反应:与偏头痛治疗相关。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-02-10 DOI: 10.1017/S1740925X11000172

Alice de Corato, Alessandro Capuano, Diego Currò, Giuseppe Tringali, Pierluigi Navarra, Cinzia Dello Russo

{"title":"Trigeminal satellite cells modulate neuronal responses to triptans: relevance for migraine therapy.","authors":"Alice de Corato, Alessandro Capuano, Diego Currò, Giuseppe Tringali, Pierluigi Navarra, Cinzia Dello Russo","doi":"10.1017/S1740925X11000172","DOIUrl":"https://doi.org/10.1017/S1740925X11000172","url":null,"abstract":"In the present paper, we have further developed an in vitro model to study neuronal-glial interaction at trigeminal level by characterizing the effects of conditioned medium (CM) collected from activated primary cultures of satellite glial cells (SGCs) on calcitonin gene-related peptide (CGRP) release from rat trigeminal neurons. Moreover, we investigated whether such release is inhibited by a clinically relevant anti-migraine drug, sumatriptan. CM effects were tested on trigeminal neuronal cultures in different conditions of activation and at different time points. Long-term exposures of trigeminal neurons to CM increased directly neuronal CGRP release, which was further enhanced by the exposure to capsaicin. In this framework, the anti-migraine drug sumatriptan was able to inhibit the evoked CGRP release from naïve trigeminal neuron cultures, as well as from trigeminal cultures pre-exposed for 30 min to CM. On the contrary, sumatriptan failed to inhibit evoked CGRP release from trigeminal neurons after prolonged (4 and 8 h) pre-exposures to CM. These findings were confirmed in co-culture experiments (neurons and SGCs), where activation of SGCs or a bradykinin priming were used. Our data demonstrate that SGCs activation could influence neuronal excitability, and that this event affects the neuronal responses to triptans.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"7 2-4","pages":"109-16"},"PeriodicalIF":0.0,"publicationDate":"2011-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X11000172","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30449290","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: 6

Evidence of microglial activation in autism and its possible role in brain underconnectivity. 自闭症中小胶质细胞激活的证据及其在大脑连接不足中的可能作用。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-07-06 DOI: 10.1017/S1740925X12000142

Juan I Rodriguez, Janet K Kern

引用次数: 159

Direct and glia-mediated effects of GABA on development of central olfactory neurons. GABA对中枢嗅觉神经元发育的直接和胶质介导作用。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-07-06 DOI: 10.1017/S1740925X12000075

Heather S Mallory, Nicholas J Gibson, Jon H Hayashi, Alan J Nighorn, Lynne A Oland

{"title":"Direct and glia-mediated effects of GABA on development of central olfactory neurons.","authors":"Heather S Mallory, Nicholas J Gibson, Jon H Hayashi, Alan J Nighorn, Lynne A Oland","doi":"10.1017/S1740925X12000075","DOIUrl":"https://doi.org/10.1017/S1740925X12000075","url":null,"abstract":"Previously studied for its role in processing olfactory information in the antennal lobe, GABA also may shape development of the olfactory pathway, acting either through or on glial cells. Early in development, the dendrites of GABAergic neurons extend to the glial border that surrounds the nascent olfactory lobe neuropil. These neuropil glia express both GABAA and GABAB receptors, about half of the glia in acute cultures responded to GABA with small outward currents, and about a third responded with small transient increases in intracellular calcium. The neuronal classes that express GABA in vivo, the local interneurons and a subset of projection neurons, also do so in culture. Exposure to GABA in culture increased the size and complexity of local interneurons, but had no effect on glial morphology. The presence of glia alone did not affect neuronal morphology, but in the presence of both glia and GABA, the growth-enhancing effects of GABA on cultured antennal lobe neurons were eliminated. Contact between the glial cells and the neurons was not necessary. Operating in vivo, these antagonistic effects, one direct and one glia mediated, could help to sculpt the densely branched, tufted arbors that are characteristic of neurons innervating olfactory glomeruli.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"7 2-4","pages":"143-61"},"PeriodicalIF":0.0,"publicationDate":"2011-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X12000075","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30820127","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: 1

Involvement of calcitonin gene-related peptide and CCL2 production in CD40-mediated behavioral hypersensitivity in a model of neuropathic pain. 在神经性疼痛模型中，降钙素基因相关肽和CCL2的产生参与cd40介导的行为超敏反应。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-03-01 DOI: 10.1017/S1740925X12000026

Jennifer T Malon, Swathi Maddula, Harmony Bell, Ling Cao

{"title":"Involvement of calcitonin gene-related peptide and CCL2 production in CD40-mediated behavioral hypersensitivity in a model of neuropathic pain.","authors":"Jennifer T Malon, Swathi Maddula, Harmony Bell, Ling Cao","doi":"10.1017/S1740925X12000026","DOIUrl":"https://doi.org/10.1017/S1740925X12000026","url":null,"abstract":"The neuropeptide calcitonin gene-related peptide (CGRP) is known to play a pro-nociceptive role after peripheral nerve injury upon its release from primary afferent neurons in preclinical models of neuropathic pain. We previously demonstrated a critical role for spinal cord microglial CD40 in the development of spinal nerve L5 transection (L5Tx)-induced mechanical hypersensitivity. Herein, we investigated whether CGRP is involved in the CD40-mediated behavioral hypersensitivity. First, L5Tx was found to significantly induce CGRP expression in wild-type (WT) mice up to 14 days post-L5Tx. This increase in CGRP expression was reduced in CD40 knockout (KO) mice at day 14 post-L5Tx. Intrathecal injection of the CGRP antagonist CGRP8-37 significantly blocked L5Tx-induced mechanical hypersensitivity. In vitro, CGRP induced glial IL-6 and CCL2 production, and CD40 stimulation added to the effects of CGRP in neonatal glia. Further, there was decreased CCL2 production in CD40 KO mice compared to WT mice 21 days post-L5Tx. However, CGRP8-37 did not significantly affect spinal cord CCL2 production following L5Tx in WT mice. Altogether, these data suggest that CD40 contributes to the maintenance of behavioral hypersensitivity following peripheral nerve injury in part through two distinct pathways, the enhancement of CGRP expression and spinal cord CCL2 production.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"7 2-4","pages":"117-28"},"PeriodicalIF":0.0,"publicationDate":"2011-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X12000026","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30495528","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: 18

ATP derived from astrocytes modulates memory in the chick. 星形胶质细胞产生的ATP调节小鸡的记忆。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-07-06 DOI: 10.1017/S1740925X12000117

Marie E Gibbs, Maria Shleper, Tomris Mustafa, Geoffrey Burnstock, David N Bowser

{"title":"ATP derived from astrocytes modulates memory in the chick.","authors":"Marie E Gibbs, Maria Shleper, Tomris Mustafa, Geoffrey Burnstock, David N Bowser","doi":"10.1017/S1740925X12000117","DOIUrl":"https://doi.org/10.1017/S1740925X12000117","url":null,"abstract":"Memory consolidation in a discriminative bead pecking task is modulated by endogenous adenosine triphosphate (ATP) acting at purinergic receptors in the hippocampus. Consolidation, from short- to intermediate- to long-term memory during two distinct periods following training, was blocked by the non-selective P2 purinergic receptor antagonist PPADS (pyridoxal phosphate-6-azo(benzene-2,4-disulphonic acid) tetrasodium salt hydrate and the specific P2Y1 receptor antagonist MRS2179. Direct injections of the ATP agonists (ATPγS and ADPβS) potentiated memory consolidation and the effect of ADPβS was blocked by MRS2179, suggesting an important role of ATP on memory consolidation via the P2Y1 receptor in the chick hippocampus. Incubation of astrocytes with ATPγS and ADPβS resulted in the increase of intracellular calcium ([Ca2+]i), the latter being blocked by MRS2179 suggesting a specific role for P2Y1 receptors in the calcium response. This response was prevented by blocking astrocytic oxidative metabolism with fluoroacetate. We argue that the source of the ATP acting on neuronal P2Y1 receptors is most likely to be astrocytes. Thrombin selectively increases [Ca2+]i in astrocytes but not in neurones. The main findings of the present study are: (a) astrocytic [Ca2+]i plays an important role in the consolidation of short-term to long-term memory; and (b) ATP released from chick astrocytes during learning modulates neuronal activity through astrocytic P2Y1 receptors.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"7 2-4","pages":"177-86"},"PeriodicalIF":0.0,"publicationDate":"2011-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X12000117","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30819688","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: 18

TSPO-specific ligand vinpocetine exerts a neuroprotective effect by suppressing microglial inflammation. tspo特异性配体长春西汀通过抑制小胶质细胞炎症发挥神经保护作用。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-07-06 DOI: 10.1017/S1740925X12000129

Yan-Yin Zhao, Jie-Zhong Yu, Qin-Ying Li, Cun-Gen Ma, Chuan-Zhen Lu, Bao-Guo Xiao

{"title":"TSPO-specific ligand vinpocetine exerts a neuroprotective effect by suppressing microglial inflammation.","authors":"Yan-Yin Zhao, Jie-Zhong Yu, Qin-Ying Li, Cun-Gen Ma, Chuan-Zhen Lu, Bao-Guo Xiao","doi":"10.1017/S1740925X12000129","DOIUrl":"https://doi.org/10.1017/S1740925X12000129","url":null,"abstract":"Vinpocetine has long been used for cerebrovascular disorders and cognitive impairment. Based on the evidence that the translocator protein (TSPO, 18 kDa) was expressed in activated microglia, while Vinpocetine was able to bind TSPO, we explored the role of Vinpocetine on microglia treated with lipopolysaccharide (LPS) and oxygen-glucose deprivation (OGD) in vitro. Our results show that both LPS and OGD induced the up-regulation of TSPO expression on BV-2 microglia by RT-PCR, western blot and immunocytochemistry. Vinpocetine inhibited the production of nitrite oxide and inflammatory factors such as interleukin-1β (IL-1β), IL-6 and tumour necrosis factor-α (TNF-α) in BV-2 microglia, in which cells were treated with LPS or exposed to OGD, regardless of the time Vinpocetine was added. Next, we measured cell death-related molecules Akt, Junk and p38 as well as inflammation-related molecules nuclear factor-κB (NF-κB) and activator protein-1 (AP-1). Vinpocetine did not change cell death-related molecules, but inhibited the expression of NF-κB and AP-1 in LPS-stimulated microglia, indicating that Vinpocetine has an anti-inflammatory effect by partly targeting NF-κB/AP-1. Next, conditioned medium from Vinpocetine-treated microglia protected from primary neurons. As compared with in vitro, the administration of Vinpocetine in hypoxic mice also inhibited inflammatory molecules, indicating that Vinpocetine as a unique anti-inflammatory agent may be beneficial for the treatment of neuroinflammatory diseases.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"7 2-4","pages":"187-97"},"PeriodicalIF":0.0,"publicationDate":"2011-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X12000129","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30820887","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: 58

Analysis of glutathione S-transferase genes polymorphisms and the risk of schizophrenia in a sample of Iranian population. 伊朗人群谷胱甘肽s -转移酶基因多态性与精神分裂症风险分析。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-07-06 DOI: 10.1017/S1740925X12000130

Farah Lotfi Kashani, Dor Mohammad Kordi-Tamandani, Roya Sahranavard, Mohammad Hashemi, Farzaneh Kordi-Tamandani, Adam Torkamanzehi

{"title":"Analysis of glutathione S-transferase genes polymorphisms and the risk of schizophrenia in a sample of Iranian population.","authors":"Farah Lotfi Kashani, Dor Mohammad Kordi-Tamandani, Roya Sahranavard, Mohammad Hashemi, Farzaneh Kordi-Tamandani, Adam Torkamanzehi","doi":"10.1017/S1740925X12000130","DOIUrl":"https://doi.org/10.1017/S1740925X12000130","url":null,"abstract":"Glutathione S-transferases (GSTs) are major intracellular antioxidants, which, impaired in their function, are involved in the progress of schizophrenia (SCZ). The aim of this case-control study was to investigate the association between the polymorphism of glutathione S-transferases M1 (GSTM1), T1 (GSTT1), the glutathione S-transferase P1 gene (GSTP1) and SCZ. We isolated genomic DNA from peripheral blood of 93 individuals with SCZ and 99 healthy control subjects' genotypes analyzing them for GSTM1, GSTT1 and GSTP1 using polymerase chain reaction. The analysis of the gene-gene interaction between GSTs indicated that the magnitude of the association was greater for the combined AG/GSTT1 & GSTM1 genotypes (OR = 2.51; 95% CI: 1.13-5.63, P = 0.02). The AG and combined AG + GG genotypes of GSTP1 increased the risk of SCZ (OR = 1.83; 95% CI: 0.94-3.75 and OR = 1.71; 95% CI: 0.92-3.19, respectively). The genotypes of GSTT/NULL, NULL/GSTM and NULL/NULL increased the risk of SCZ (OR = 2.05; 95% CI: 0.9-4.74; OR = 2.0; 95% CI: 1.68-2.31; and OR = 1.8; 95% CI: 0.57-2.46, respectively). The present study supports previous data that suggest that impairment in the function of GSTs genes may increase the risk of SCZ.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"7 2-4","pages":"199-203"},"PeriodicalIF":0.0,"publicationDate":"2011-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X12000130","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30820894","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: 13

Exposure to environmental enrichment prior to a cerebral cortex stab wound attenuates the postlesional astroglia response in rats. 在大鼠的大脑皮层刺伤之前暴露于环境富集减弱了伤后星形胶质细胞的反应。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-07-06 DOI: 10.1017/S1740925X12000099

Ximena A Lanosa, Ignacio Santacroce, Jorge A Colombo

{"title":"Exposure to environmental enrichment prior to a cerebral cortex stab wound attenuates the postlesional astroglia response in rats.","authors":"Ximena A Lanosa, Ignacio Santacroce, Jorge A Colombo","doi":"10.1017/S1740925X12000099","DOIUrl":"https://doi.org/10.1017/S1740925X12000099","url":null,"abstract":"Modulation of astroglial components involved in reactive postlesional responses in the rat cerebral cortex was analyzed following exposure to environmental enrichment (EE) condition prior to injury. For this purpose, changes in % immunoreactive (IR) area of GFAP, vimentin, EAAT1 and ezrin were evaluated in the perilesional zone after placing a cortical stab wound in the visual cerebral cortex of adult rats. GFAP-IR postlesional reactive astrocytosis in the perilesional cortex was significantly lower in the animal group exposed to EE during postnatal development. This GFAP-IR reaction seems to be associated with existing astroglia, because neither BrdU- nor endogenous Ki-67-labeled nuclei were found in the perilesional cortex analyzed. Increased ezrin-IR area in the visual cortex of rats exposed to EE condition suggests the formation of new synapses or the enhancement of astroglial involvement in the existing ones. No effects of EE were found on either EAAT1- or vimentin-IR area. Results suggest that exposure to EE conditions prior to injury attenuates the postlesional astroglia GFAP-response in the perilesional cortex of rats. Whether this attenuated postlesional astroglia GFAP-response promotes or not protective effects on the cortical neuropil remains to be explored in futures studies.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"7 2-4","pages":"163-75"},"PeriodicalIF":0.0,"publicationDate":"2011-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X12000099","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30819319","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: 7

The effects of L-NAME on neuronal NOS and SOD1 expression in the DRG-spinal cord network of axotomised Thy 1.2 eGFP mice. L-NAME对Thy 1.2 eGFP小鼠腋窝切除后drg -脊髓网络神经元NOS和SOD1表达的影响。

Neuron glia biology Pub Date : 2011-05-01 Epub Date: 2012-05-22 DOI: 10.1017/S1740925X12000051

Matthew J G Bradman, Richard Morris, Anne McArdle, Malcolm J Jackson, Thimmasettappa Thippeswamy

{"title":"The effects of L-NAME on neuronal NOS and SOD1 expression in the DRG-spinal cord network of axotomised Thy 1.2 eGFP mice.","authors":"Matthew J G Bradman, Richard Morris, Anne McArdle, Malcolm J Jackson, Thimmasettappa Thippeswamy","doi":"10.1017/S1740925X12000051","DOIUrl":"https://doi.org/10.1017/S1740925X12000051","url":null,"abstract":"Nitric oxide (NO) plays an important role in pathophysiology of the nervous system. Copper/zinc superoxide dismutase (SOD1) reacts with superoxide, which is also a substrate for NO, to provide antioxidative protection. NO production is greatly altered following nerve injury, therefore we hypothesised that SOD1 and NO may be involved in modulating axotomy responses in dorsal root ganglion (DRG)-spinal network. To investigate this interaction, adult Thy1.2 enhanced membrane-bound green fluorescent protein (eGFP) mice underwent sciatic nerve axotomy and received NG-nitro- <l-arginine methylester (L-NAME) or vehicle 7-9 days later. L4-L6 spinal cord and DRG were harvested for immunohistochemical analyses. Effect of injury was confirmed by axotomy markers; small proline-rich repeat protein 1A (SPRR1A) was restricted to ipsilateral neuropathology, while Thy1.2 eGFP revealed also contralateral crossover effects. L-NAME, but not axotomy, increased neuronal NO synthase (nNOS) and SOD1 immunoreactive neurons, with no colocalisation, in a lamina-dependent manner in the dorsal horn of the spinal cord. Axotomy and/or L-NAME had no effect on total nNOS+ and SOD1+ neurons in DRG. However, L-NAME altered SOD1 expression in subsets of axotomised DRG neurons. These findings provide evidence for differential distribution of SOD1 and its modulation by NO, which may interact to regulate axotomy-induced changes in DRG-spinal network.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"7 2-4","pages":"129-41"},"PeriodicalIF":0.0,"publicationDate":"2011-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X12000051","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30632286","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

The role of microglial mtDNA damage in age-dependent prolonged LPS-induced sickness behavior. 小胶质细胞mtDNA损伤在年龄依赖性延长脂多糖诱导的疾病行为中的作用。

Neuron glia biology Pub Date : 2011-02-01 Epub Date: 2011-10-28 DOI: 10.1017/S1740925X1100010X

Hiroshi Nakanishi, Yoshinori Hayashi, Zhou Wu

{"title":"The role of microglial mtDNA damage in age-dependent prolonged LPS-induced sickness behavior.","authors":"Hiroshi Nakanishi, Yoshinori Hayashi, Zhou Wu","doi":"10.1017/S1740925X1100010X","DOIUrl":"https://doi.org/10.1017/S1740925X1100010X","url":null,"abstract":"Microglia are the main cellular source of oxidation products and inflammatory molecules in the brain during aging. The accumulation of mitochondrial DNA (mtDNA) oxidative damage in microglia during aging results in the increased production of reactive oxygen species (ROS). The increased intracellular ROS, in turn, activates a redox-sensitive nuclear factor-κB (NF-κB) to provoke excessive neuroinflammation, resulting in memory deficits and the prolonged behavioral consequence of infection. Besides its role in regulating the gene copy number, mitochondrial transcription factor A (TFAM) is closely associated with the stabilization of mtDNA structures. Lipopolysaccharide (LPS) induces the generation of ROS from the actively respirating mitochondria as well as NADPH oxidase, and leads to the subsequent activation of the NF-κB-dependent inflammatory pathway in aging microglia. The overexpression of human TFAM improves the age-dependent prolonged LPS-induced sickness behaviors by ameliorating the mtDNA damage and reducing the resultant redox-regulated inflammatory responses. Therefore, 'microglia-aging' plays important roles in the age-dependent enhanced behavioral consequences of infection.","PeriodicalId":19153,"journal":{"name":"Neuron glia biology","volume":"7 1","pages":"17-23"},"PeriodicalIF":0.0,"publicationDate":"2011-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1017/S1740925X1100010X","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30092559","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: 25