Changing Face of Microglia

Graeber, Manuel B.

doi:10.1126/science.1190929

Cited by 536 publications

(420 citation statements)

References 53 publications

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“…On the basis of these observations, researchers have sought a potential explanation for why an organism might expend considerable energy to continuously scan the neuropil under homeostatic conditions. As a result, several groups have argued that microglia might have an essential role in monitoring synaptic activity Graeber, 2010;Kettenmann et al, 2013;. In support of this hypothesis, ultrastructural analysis in mice has revealed that microglial processes make direct contact not only with axon terminals and dendritic spines but also astrocytes and their perisynaptic processes that ensheath dendritic branches (Tremblay et al, 2010).…”

Section: Microgliamentioning

confidence: 98%

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

Lacagnina

Rivera

Bilbo

2016

Neuropsychopharmacol

218

170

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Drugs of abuse cause persistent alterations in synaptic plasticity that may underlie addiction behaviors. Evidence suggests glial cells have an essential and underappreciated role in the development and maintenance of drug abuse by influencing neuronal and synaptic functions in multifaceted ways. Microglia and astrocytes perform critical functions in synapse formation and refinement in the developing brain, and there is growing evidence that disruptions in glial function may be implicated in numerous neurological disorders throughout the lifespan. Linking evidence of function in health and under pathological conditions, this review will outline the glial and neuroimmune mechanisms that may contribute to drug-abuse liability, exploring evidence from opioids, alcohol, and psychostimulants. Drugs of abuse can activate microglia and astrocytes through signaling at innate immune receptors, which in turn influence neuronal function not only through secretion of soluble factors (eg, cytokines and chemokines) but also potentially through direct remodeling of the synapses. In sum, this review will argue that neural-glial interactions represent an important avenue for advancing our understanding of substance abuse disorders.

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Section: Microgliamentioning

confidence: 98%

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

Lacagnina

Rivera

Bilbo

2016

Neuropsychopharmacol

218

170

View full text Add to dashboard Cite

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“…Microglial activation may also be a response to neuronal loss as well as to neuronal dysfunction and their extremely low activation threshold results in their almost universal involvement in even subtle brain pathologies [41]. So in neurodegenerative diseases, widespread microglial activation may reflect widespread neuronal dysfunction in addition to the more apparent alterations of synapses.…”

Section: Alzheimer's Diseasementioning

confidence: 99%

“…Although microglia can express ''immune molecules'', this is not synonymous with inflammation, since these molecules can have CNS-specific roles independent of their roles in the immune or inflammatory response [41]. Similarly, molecules known to neurobiology, including gamma amino butyric acid and the lens protein alpha B crystallin can have intriguing and distinct functions in the immune system [47].…”

Section: Role Of Microglia In Normal Brainmentioning

confidence: 99%

Role of microglia in CNS inflammation

2011

Self Cite

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There is increasing confusion about the meaning of the terms inflammation, neuroinflammation, and microglial inflammation. We aim in this review to achieve greater clarity regarding these terms, which are essential for our understanding of the role of microglia in CNS inflammatory conditions. The important concept of sterile inflammation is explained against the backdrop of classical inflammation, and its key differences from what researchers refer to when they use the terms neuroinflammation and microglial inflammation are illustrated. We propose to replace the term “neuroinflammation” with “microglial activation” or “CNS pseudo‐inflammation”, if microglial activation does not suffice. In addition, we recommend abandoning the terms “microglial inflammation” and “inflamed microglia” because of the lack of a clear concept behind them.

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“…They actively move their branched processes to sense pathological alterations or disturbances to ultimately maintain CNS homeostasis [1][2][3][4]. Once abnormalities are detected, microglia dramatically transform into a reactive phenotype through a progressive series of cellular and molecular changes, including morphological hypertrophy, proliferation, and the expression of various genes [3,5].…”

Section: Introductionmentioning

confidence: 99%

IRF8 is a transcriptional determinant for microglial motility

Masuda

Nishimoto

Tomiyama

et al. 2014

Purinergic Signalling

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Microglia, the resident immune cells of the central nervous system, are constitutively mobile cells that undergo rapid directional movement toward sites of tissue disruption. However, transcriptional regulatory mechanisms of microglial motility remain unknown. In the present study, we show that interferon regulatory factor-8 (IRF8) regulates microglial motility. We found that ATP and complement component, C5a, induced chemotaxis of IRF8 wild-type microglia. However, these responses were markedly suppressed in microglia lacking IRF8 (Irf8 −/− ). In a consistent manner, phosphorylation of Akt (which plays a crucial role in ATP-induced chemotaxis) was abolished in Irf8 −/− microglia. Real-time polymerase chain reaction analysis revealed that motility-related microglial genes such as P2Y 12 receptor were significantly suppressed in Irf8 −/− microglia. Furthermore, Irf8 −/− microglia exhibited a differential expression pattern of nucleotidedegrading enzymes compared with their wild-type counterparts. Overall, our findings suggest that IRF8 may regulate microglial motility via the control of microglial gene expression.

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Changing Face of Microglia

Cited by 536 publications

References 53 publications

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

Glial and Neuroimmune Mechanisms as Critical Modulators of Drug Use and Abuse

Role of microglia in CNS inflammation

IRF8 is a transcriptional determinant for microglial motility

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