Physiology of Microglia

被引:2700
作者
Kettenmann, Helmut [1 ]
Hanisch, Uwe-Karsten
Noda, Mami
Verkhratsky, Alexei
机构
[1] Max Delbruck Ctr Mol Med, Berlin, Germany
关键词
CENTRAL-NERVOUS-SYSTEM; TUMOR-NECROSIS-FACTOR; TOLL-LIKE RECEPTORS; VASOACTIVE-INTESTINAL-PEPTIDE; CULTURED RAT MICROGLIA; FOCAL CEREBRAL-ISCHEMIA; PROTEASE-ACTIVATED RECEPTORS; NF-KAPPA-B; COLONY-STIMULATING FACTOR; TRAUMATIC BRAIN-INJURY;
D O I
10.1152/physrev.00011.2010
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Kettenmann H, Hanisch U-K, Noda M, Verkhratsky A. Physiology of Microglia. Physiol Rev 91: 461-553, 2011; doi:10.1152/physrev.00011.2010.-Microglial cells are the resident macrophages in the central nervous system. These cells of mesodermal/mesenchymal origin migrate into all regions of the central nervous system, disseminate through the brain parenchyma, and acquire a specific ramified morphological phenotype termed "resting microglia." Recent studies indicate that even in the normal brain, microglia have highly motile processes by which they scan their territorial domains. By a large number of signaling pathways they can communicate with macroglial cells and neurons and with cells of the immune system. Likewise, microglial cells express receptors classically described for brain-specific communication such as neurotransmitter receptors and those first discovered as immune cell-specific such as for cytokines. Microglial cells are considered the most susceptible sensors of brain pathology. Upon any detection of signs for brain lesions or nervous system dysfunction, microglial cells undergo a complex, multistage activation process that converts them into the "activated microglial cell." This cell form has the capacity to release a large number of substances that can act detrimental or beneficial for the surrounding cells. Activated microglial cells can migrate to the site of injury, proliferate, and phagocytose cells and cellular compartments.
引用
收藏
页码:461 / 553
页数:93
相关论文
共 1066 条
[61]  
BEZPROZVANNY I, 1995, J MEMBRANE BIOL, V145, P205
[62]   CXCR4-activated astrocyte glutamate release via TNFa: amplification by microglia triggers neurotoxicity [J].
Bezzi, P ;
Domercq, M ;
Brambilla, L ;
Galli, R ;
Schols, D ;
De Clercq, E ;
Vescovi, A ;
Bagetta, G ;
Kollias, G ;
Meldolesi, J ;
Volterra, A .
NATURE NEUROSCIENCE, 2001, 4 (07) :702-710
[63]   DAMPs, PAMPs and alarmins: all we need to know about danger [J].
Bianchi, Marco E. .
JOURNAL OF LEUKOCYTE BIOLOGY, 2007, 81 (01) :1-5
[64]   Pathophysiological roles of extracellular nucleotides in glial cells: differential expression of purinergic receptors in resting and activated microglia [J].
Bianco, F ;
Fumagalli, M ;
Pravettoni, E ;
D'Ambrosi, N ;
Volonte, C ;
Matteoli, M ;
Abbracchio, MP ;
Verderio, C .
BRAIN RESEARCH REVIEWS, 2005, 48 (02) :144-156
[65]   Astrocyte-derived ATP induces vesicle shedding and IL-1β release from microglia [J].
Bianco, F ;
Pravettoni, E ;
Colombo, A ;
Schenk, U ;
Möller, T ;
Matteoli, M ;
Verderio, C .
JOURNAL OF IMMUNOLOGY, 2005, 174 (11) :7268-7277
[66]   Neuron-microglia signaling: Chemokines as versatile messengers [J].
Biber, K. ;
Vinet, J. ;
Boddeke, H. W. G. M. .
JOURNAL OF NEUROIMMUNOLOGY, 2008, 198 (1-2) :69-74
[67]   Ischemia-induced neuronal expression of the microglia attracting chemokine secondary lymphoid-tissue chemokine (SLC) [J].
Biber, K ;
Sauter, A ;
Brouwer, N ;
Copray, SCVM ;
Boddeke, HWGM .
GLIA, 2001, 34 (02) :121-133
[68]   Expression and signaling of group I metabotropic glutamate receptors in astrocytes and microglia [J].
Biber, K ;
Laurie, DJ ;
Berthele, A ;
Sommer, B ;
Tölle, TR ;
Gebicke-Härter, PJ ;
van Calker, D ;
Boddeke, HWGM .
JOURNAL OF NEUROCHEMISTRY, 1999, 72 (04) :1671-1680
[69]   Neuronal 'On' and 'Off' signals control microglia [J].
Biber, Knut ;
Neumann, Harald ;
Inoue, Kazuhide ;
Boddeke, Hendrikus W. G. M. .
TRENDS IN NEUROSCIENCES, 2007, 30 (11) :596-602
[70]   Sodium Channel Activity Modulates Multiple Functions in Microglia [J].
Black, Joel A. ;
Liu, Shujun ;
Waxman, Stephen G. .
GLIA, 2009, 57 (10) :1072-1081