Trends in Neurosciences
Reactive astrocytes: cellular and molecular cues to biological function
Section snippets
Markers of reactive astrocytes
Over the last decade, the development of new cellular and molecular markers for astroglial cells has advanced our knowledge of neuroglial interactions occurring during development and after various types of CNS injury. In this section, we summarize an update of the available markers for the identification of activated astrocytes (Table 1).
Proximal and distal reactive astrocytes: isotropic vs anisotropic gliosis
There is now strong evidence that reactive gliosis varies qualitatively and quantitatively depending on both the nature of the injury and the microenvironment of the injury site. Over the past two decades, many studies have reported differences between astrogliosis in adult and neonatal rats. For example, the spread and/or intensity of reactive gliosis is much greater in adult than in neonatal animals. Only a few papers have focused on the heterogeneity within the reactive astroglial
Production of cytokines, neurotrophic factors and their receptors
Though it is now well documented that the expression of many cytokines and neurotrophic factors is modulated after CNS injury, the cellular origin of these factors is unclear. The amounts of LIF are increased in gliotic tissue, and it has also been suggested that LIF might modulate the post-lesional activation of astrocytes15, 16. Although it is expressed by cultured astrocytes, IGF-I is only detected in neurons in the intact CNS, and it is re-expressed in reactive astrocytes, suggesting a role
Concluding remarks
Reactive gliosis, of which astrocytes are only one element, is a very complex phenomenon, involving interactions of several cell types with neurons (Fig. 1), leading eventually to neuron survival or death, axonal regeneration or retraction. We have outlined here one aspect of astrocyte complexity and versatility: the diversity of the repertoire of markers, receptors, factors expressed, according to the age, the location and the extent of the causal injury. One key issue is that of cell-adhesion
Acknowledgements
This review was initiated while J.L. Ridet was at the Salk Institute, in the lab. of F.H. Gagel.
References (102)
J. Neuroimmunol.
(1994)- et al.
Curr. Opin. Neurobiol.
(1995) Mol. Brain Res.
(1994)- et al.
Brain Res. Bull.
(1994) - et al.
Exp. Neurol.
(1996) - et al.
Brain Res.
(1992) Neurosci. Lett.
(1988)- et al.
Trends Neurosci.
(1996) Brain Res.
(1986)- et al.
Trends Pharmacol.
(1992)