The literature reviewed above demonstrates that all cell types occurring within ischaemic regions of the mammalian central nervous system respond to such an
insult. This is hardly surprising since ischaemia will necessarily result in a marked reduction of the level of major substrates for energy metabolism throughout the ischaemia area. But it is also clear that there are differences in either or both the rate and degree of response by different cells.
Until recently it has been suggested that astrocytes respond most rapidly. However, this impression seems to have been based upon changes in their morphology. Use of molecular techniques, however, now indicates that microglia and smooth muscle in the tunica intima of parenchymal arteries respond most quickly to an ischaemic insult. In the case of microglia, changes occur in their physiology and biochemistry before there is any ultrastructural indication of a response. Ultrastructural changes in microglia occur in the same postischaemic time frame as responses by astrocytes. At the other extreme, the concept that oligodendrocytes do not respond to an ischaemic episode has not been substantiated. Rather there is a response by medium-light oligodendrocytes within a long-term postischaemic time frame. However, the significance of this response has not yet been elucidated.
It is also clear, and has been established for some time now, that some neurons are susceptible to relatively short periods of ischaemia while others are not. Initially there are changes in the biochemical activity of neurons, in parallel with other cell types, which precede progressive tissue destruction. Although both types of neurons demonstrate similar morphological responses initially, susceptible neurons, perhaps due to differences in the biochemistry of some structural cytoskeletal components, for example, enter a postischaemic pathological cascade culminating in their death between 2 and 4 days and later after the ischaemic episode. However, despite a great deal of work which has attempted to unravel these complex intracellular processes, there is still not a clear and simple overview available. It is also apparent that for reperfusion to be beneficial after a period of ischaemia it must be reestablished very early after an ischaemic episode. A delay in the reestablishment of reperfusion may in fact exacerbate degenerative neuronal and other cell sequelae. In addition, although circumstantial evidence exists that other nonsusceptible neurons recover from a short-term ischaemic episode, there is still a lack of good quality, quantitative experimental data to substantiate this impression.
Thus, a number of biochemical/biological factors which certainly differ from neuron to neuron and probably between different subtypes of other cells within the central nervous system, govern the specific ischaemic vulnerability of each cell. Since the interval available for the reversal or inhibition of biochemical processes initiated during the ischaemic episode may in fact be quite short, it is clear that analysis of structural changes will provide little insight but rather will reflect the end-point of such processes. Therefore, it may be more rewarding to therapeutically interfere with the variety of complex biochemical changes that essentially determine the fate of the ischaemic tissue while acknowledging that no single cell population can be analysed in isolation; rather, there is a very complex interaction at the molecular level between all cell types within the central nervous system. This complex interaction is disrupted to differing degrees in different types of cell by an ischaemic episode.
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