Preface

This Special Issue of the International Journal of Developmental Neuroscience is representative of the most active area of research in the field of astrocyte response to injury. In this respect (response to injury), astrocytes may be compared to fibroblasts elsewhere in the body in that, like fibroblasts, they are less vulnerable than parenchymal cells and react to parenchymal injury, if one considers neurons as the parenchyma of the brain. The histology of astrocyte response to injury was well known at the beginning of this century but little progress was made for about 70 years. This was probably due to the fact that--with electron microscopy being the most notable exception--the experimental methodology evolved slowly during this time. As can be noted in this Special Issue, a wealth of methods are now utilized which were unavailable to traditional neurohistologists. The new methods have produced results which have considerably changed our concept of the astrocyte response to injury. For example, a traditional neuropathologist may find it somewhat surprising that fibrous gliosis is, to a large extent, not an irreversible phenomenon. Also, he/she may be somewhat bewildered by the extraordinary complexity of events underlying simple statements found in neuropathology textbooks such as "astrocytes react to all noxae which damage neurons". Another important consequence of the improved methodology is the realization that the brain is not unique with respect to several pathological processes such that research about other systems (e.g. the immune system and inflammation) has greatly facilitated research in neuropathology. This is of particular significance since most investigators in the neurosciences are involved in neuronspecific processes such as neurotransmitters and their receptors, and this leaves fewer scientists to study problems more directly related to general cell biology. If astrocytes behave as the connective tissue of the brain in the reparative processes that follow brain injury, from the perspective of functional interactions, they appear to form a single tissue. As evidenced in this Special Issue, still very little is known concerning the disruption of such functional interactions that may occur where astrocytes respond to injury. An example would be the glutamate uptake system in astrocytes reacting to neuronal injury. If uptake is enhanced, the neurons would get extra protection against the toxic effect of the excitatory neurotransmitter. Alternatively, the uptake system may be impaired, considering that the astrocyte machinery is switched to other tasks such as cell division and fibrillogenesis. Also, the possibility that astrocytes may be the primum movens in brain dysfunction, the "primary" gliosis of traditional neuropathology, has not been completely disproved. In other words, the reader should be aware of the fact that other special issues on this topic may be forthcoming.