Abstract
The monthly intracisternal inoculation of aluminum chloride (AlCl 3) to young adult New Zealand white rabbits induces motor neuron degeneration marked by intraneuronal neurofilamentous aggregates similar to that observed in amyotrophic lateral sclerosis (ALS). However, in contrast to ALS, this process occurs in the experimental paradigm in the absence of a glial response. In addition, whereas ALS is a fatal disorder, the cessation of aluminum exposure leads to both clinical and neuropathological recovery. Because microglia can influence neuronal regeneration, we have examined the effect of both acute and chronic aluminum exposure on microglial activation in vivo. We have studied microglial morphology in young adult New Zealand white rabbits receiving either single (1000 μg) or repeated sublethal (100 μg monthly) intracisternal inoculums of AlCl 3. In addition, rabbits receiving 1000 μg AlCl 3 inoculums were studied following an unilateral sciatic axotomy 48 h prior to the AlCl 3 exposure. Our studies demonstrate that microglial activation in vivo is inhibited by AlCl 3 exposure, and that a correlation exists between the extent of microglia suppression and the potential for recovery. This suggests that microglial activation is an important determinant of neuronal injury.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call