Rat retinal microglial cells under normal conditions, after optic nerve section, and after optic nerve section and intravitreal injection of trophic factors or macrophage inhibitory factor

2007 ◽  
Vol 501 (6) ◽  
pp. 866-878 ◽  
Author(s):  
Paloma Sobrado-Calvo ◽  
Manuel Vidal-Sanz ◽  
María P. Villegas-Pérez
Neuroscience ◽  
2004 ◽  
Vol 126 (3) ◽  
pp. 775-783 ◽  
Author(s):  
C. Gargini ◽  
S. Bisti ◽  
G.C. Demontis ◽  
K. Valter ◽  
J. Stone ◽  
...  

2019 ◽  
Vol 25 (21) ◽  
pp. 2375-2393 ◽  
Author(s):  
Yun Yuan ◽  
Chunyun Wu ◽  
Eng-Ang Ling

Background: Microglia play a pivotal role in maintaining homeostasis in complex brain environment. They first exist as amoeboid microglial cells (AMCs) in the developing brain, but with brain maturation, they transform into ramified microglial cells (RMCs). In pathological conditions, microglia are activated and have been classified into M1 and M2 phenotypes. The roles of AMCs, RMCs and M1/M2 microglia phenotypes especially in pathological conditions have been the focus of many recent studies. Methods: Here, we review the early development of the AMCs and RMCs and discuss their specific functions with reference to their anatomic locations, immunochemical coding etc. M1 and M2 microglia phenotypes in different neuropathological conditions are also reviewed. Results: Activated microglia are engaged in phagocytosis, production of proinflammatory mediators, trophic factors and synaptogenesis etc. Prolonged microglia activation, however, can cause damage to neurons and oligodendrocytes. The M1 and M2 phenotypes featured prominently in pathological conditions are discussed in depth. Experimental evidence suggests that microglia phenotype is being modulated by multiple factors including external and internal stimuli, local demands, epigenetic regulation, and herbal compounds. Conclusion: Prevailing views converge that M2 polarization is neuroprotective. Thus, proper therapeutic designs including the use of anti-inflammatory drugs, herbal agents may be beneficial in suppression of microglial activation, especially M1 phenotype, for amelioration of neuroinflammation in different neuropathological conditions. Finally, recent development of radioligands targeting 18 kDa translocator protein (TSPO) in activated microglia may hold great promises clinically for early detection of brain lesion with the positron emission tomography.


Development ◽  
1988 ◽  
Vol 102 (3) ◽  
pp. 479-488
Author(s):  
M.F. Humphrey ◽  
C.A.O. Stuermer

The tectal pathways of regenerating goldfish optic axons are abnormal but not random. The relative proportion of temporal axons is highest in rostral tectum (65%) drops in midtectum (31%) and is very low in caudal tectum (4%). By contrast, nasal axons proceed into caudal tectum and are therefore relatively evenly distributed throughout the tectum. In this study, we have tested whether temporal axons are confined to rostral tectum by the presence of nasal axons in caudal tectum or whether they have a preference for rostral tectum regardless of other axons. We similarly tested whether nasal axons would grow preferentially into caudal tectum in the absence of temporal axons. At the time of optic nerve section either the nasal or temporal half retina was removed. Either 35 or 70 days after nerve section, the regenerating optic axons were labelled with HRP and both their pathways and distribution determined in DAB-reacted tectal wholemounts. In the absence of nasal axons, the relative density of temporal axons in rostral, mid and caudal tectum was 70%, 28% and 2%, respectively. The corresponding values for nasal axons, in the absence of temporal axons, were 30%, 40% and 30%, respectively. Thus, the overall distribution of nasal and temporal axons in the half retinal regenerates was similar to that of whole retinal regenerates, demonstrating that the retinotopic preferences of the axons were not dependent upon interaxonal interactions. Thus, nasal and temporal axons obviously discriminate between rostral and caudal tectum despite pathway disorganization and the absence of axons from the opposite hemiretina. This is consistent with axonal growth being under the influence of positional markers in tectum.


1989 ◽  
Vol 9 (4) ◽  
pp. 1263-1272 ◽  
Author(s):  
G Carmignoto ◽  
L Maffei ◽  
P Candeo ◽  
R Canella ◽  
C Comelli

1988 ◽  
Vol 20 ◽  
pp. 65
Author(s):  
P. Candeo ◽  
G. Carmignoto ◽  
L. Maffei ◽  
R. Canella ◽  
C. Comelli

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