Infusion of cytosine‐arabinoside into the cerebrospinal fluid of the rat brain inhibits the microglial cell proliferation after hypoglossal nerve injury

Abstract

The present study describes a method to inhibit selectively the microglial cell proliferation following peripheral nerve injury. Continuous infusion of cytosine-arabinoside (ARA-C) from an osmotic minipump to the fourth ventricle or cisterna magna completely blocks the proliferation of microglial cells that normally occurs following hypoglossal nerve transection. This treatment had no significant effect on other glial cells or on the expected morphological changes in the axotomized hypoglossal motorneurons. The method opens up new possibilities for analyzing the functional role of the axotomy-induced microglial cell reaction.

Upregulation of calcium binding protein, S100A6, in activated astrocytes is linked to glutamate toxicity

“…Interestingly, the surface area of S100A6+ profiles was significantly increased after axotomy in mice but not in rats, while GFAP+ surface area was significantly increased following axotomy in both species. There were no significant changes in the numerical densities of S100b+ astrocytes after axotomy in both species, as reported previously (Svensson and Aldskogius, 1993;. Because GFAP is commonly upregulated in the activation process of astrocytes in response to injury (Norton et al, 1992;Eng et al, 2000), it is reasonable to suppose that astrocytes are activated after axotomy in both species without cell proliferation.…”

Regeneration of Hypoglossal Nerve Axons Following Blockade of the Axotomy‐induced Microglial Cell Reaction in the Rat

“…The increase in OX42 immunoreactivity n o d y seen ipsilateral to axotomy was abolished following ARA-C infusion during the period of examination in the present study. This strongly indicates that the microglial reaction has been effectively blocked (see also Svensson and Aldskogius, 1992a). However, it should be noted that the minipump infuses ARA-C only during the first postoperative week.…”

Region-specific activation of microglial cells in the rat septal complex following fimbria-fornix transection

“…Most data on the microglial response to axotomy have been derived from studies in cranial nerves (e.g., Sjös-trand, 1971;Torvik and Søreide, 1975;Aldskogius, 1982;Svensson and Aldskogius, 1993) or peripheral nerves (e.g., Kerns and Hinsman, 1973;Cova et al, 1988;Eriksson et al, 1993;Lu and Richardson, 1993). In particular, changes in microglial cells after transection of the facial nerve were investigated extensively by Kreutzberg and coworkers (Blinzinger and Kreutzberg, 1968;Streit and Kreutzberg, 1987;Graeber et al, 1988a,b;Streit and Graeber, 1993).…”