Effect of Lipopolysaccharide on the Morphology and Integrin Immunoreactivity of Ramified Microglia in the Mouse Brain and in Cell Culture

Kloss, Christian U.A.; Bohatschek, Marion; Kreutzberg, Georg W.; Raivich, Gennadij

doi:10.1006/exnr.2000.7575

Cited by 162 publications

(137 citation statements)

References 76 publications

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“…The second possible explanation is that the ramified microglia may not appropriately reflect resting phenotype. It was reported that systemic injection of LPS activates brain microglia, but does not cause them to transform into amoeboid macrophages (Kloss et al, 2001). Recent in vivo studies also showed that ramified microglia in the normal brain carry out homeostatic surveillance, therefore, it is not justified to consider ramified microglia as resting microglia (Hanisch and Kettenmann, 2007;Nimmerjahn et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

GM1 induces p38 and microtubule dependent ramification of rat primary microglia in vitro

Park¹,

Kim²,

Jou³

et al. 2008

Brain Research

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Section: Discussionmentioning

confidence: 99%

GM1 induces p38 and microtubule dependent ramification of rat primary microglia in vitro

Park¹,

Kim²,

Jou³

et al. 2008

Brain Research

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“…However, this might either be due to a direct effect of A 2A Rs known to be present in microglia cells [41,42,216] or because A 2A R antagonists control the evolution of the severity of convulsion and associated neurotoxicity triggered by cumulative sub-threshold amygdala kindling or by kainate injection [284], which pre-date microglia recruitment. It was also recently shown that an A 2A R antagonist (SCH 58261) can prevent the hippocampal neuronal dysfunction and neurotoxicity triggered by the direct administration of lipopolyssaccharide (LPS) [285], a potent inflammatory trigger and activator of microglia cells (see e.g., [286,287]). Interestingly, SCH 58261 also attenuated the LPS-induced neuro-inflammation, as evaluated by the abolishment of LPS-induced increase in interleukin 1b levels and the recruitment of activated microglia [285].…”

Section: A 2a Receptor Blockade Confers Robust Neuroprotectionmentioning

confidence: 99%

Neuroprotection by adenosine in the brain: From A1 receptor activation to A2A receptor blockade

Cunha

2005

Purinergic Signalling

484

432

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Adenosine is a neuromodulator that operates via the most abundant inhibitory adenosine A 1 receptors (A 1 Rs) and the less abundant, but widespread, facilitatory A 2A Rs. It is commonly assumed that A 1 Rs play a key role in neuroprotection since they decrease glutamate release and hyperpolarize neurons. In fact, A 1 R activation at the onset of neuronal injury attenuates brain damage, whereas its blockade exacerbates damage in adult animals. However, there is a down-regulation of central A 1 Rs in chronic noxious situations. In contrast, A 2A Rs are up-regulated in noxious brain conditions and their blockade confers robust brain neuroprotection in adult animals. The brain neuroprotective effect of A 2A R antagonists is maintained in chronic noxious brain conditions without observable peripheral effects, thus justifying the interest of A 2A R antagonists as novel protective agents in neurodegenerative diseases such as Parkinson's and Alzheimer's disease, ischemic brain damage and epilepsy. The greater interest of A 2A R blockade compared to A 1 R activation does not mean that A 1 R activation is irrelevant for a neuroprotective strategy. In fact, it is proposed that coupling A 2A R antagonists with strategies aimed at bursting the levels of extracellular adenosine (by inhibiting adenosine kinase) to activate A 1 Rs might constitute the more robust brain neuroprotective strategy based on the adenosine neuromodulatory system. This strategy should be useful in adult animals and especially in the elderly (where brain pathologies are prevalent) but is not valid for fetus or newborns where the impact of adenosine receptors on brain damage is different.Abbreviations: Ab -b-amyloid peptide; A 1 Rs -A 1 receptors; A 2A Rs -A 2A

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“…Resident microglia in the healthy brain display a ''resting state" appearing in a downgraded phenotype, with highly ramified morphology and a low expression of membrane receptors that serve 0091 immunological functions [123]; even in this resting state microglia are highly active as shown by the high motility of their processes and protrusions observed by two-photon imaging analysis of brain in vivo ( [53,173]). Microglia are the first cell type that sense any form of disturbance of the brain and rapidly activate through a well-characterized and graded response; the inner cytoskeleton changes and the cell body becomes enlarged, bearing shorter and thicker cytoplasmic processes ( [174,218]).…”

Section: Role Of Microglia In Neurodegenerationmentioning

confidence: 99%

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

Vegeto

Benedusi

Maggi

2008

Frontiers in Neuroendocrinology

278

206

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a b s t r a c tRecent studies highlight the prominent role played by estrogens in protecting the central nervous system (CNS) against the noxious consequences of a chronic inflammatory reaction. The neurodegenerative process of several CNS diseases, including Multiple Sclerosis, Alzheimer's and Parkinson's Diseases, is associated with the activation of microglia cells, which drive the resident inflammatory response. Chronically stimulated during neurodegeneration, microglia cells are thought to provide detrimental effects on surrounding neurons. The inhibitory activity of estrogens on neuroinflammation and specifically on microglia might thus be considered as a beneficial therapeutic opportunity for delaying the onset or progression of neurodegenerative diseases; in addition, understanding the peculiar activity of this female hormone on inflammatory signalling pathways will possibly lead to the development of selected anti-inflammatory molecules. This review summarises the evidence for the involvement of microglia in neuroinflammation and the anti-inflammatory activity played by estrogens specifically in microglia.

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Effect of Lipopolysaccharide on the Morphology and Integrin Immunoreactivity of Ramified Microglia in the Mouse Brain and in Cell Culture

Cited by 162 publications

References 76 publications

GM1 induces p38 and microtubule dependent ramification of rat primary microglia in vitro

GM1 induces p38 and microtubule dependent ramification of rat primary microglia in vitro

Neuroprotection by adenosine in the brain: From A1 receptor activation to A2A receptor blockade

Estrogen anti-inflammatory activity in brain: A therapeutic opportunity for menopause and neurodegenerative diseases

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