Histochemical study of neuronal necrosis produced by intracerebral injection of diphtheria toxin

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Abstract
The intracerebral injection of diphtheria toxin in rats causes necrosis of neurons of the cerebral cortex, striatum, and cerebellum. In the course of this necrotizing lesion, neurons may be shown to develop enlarged droplets of lead sulfide, as demonstrated by the Gomori procedure for acid phosphatase. Beta-glucuronidase activity appears to be increased in early stages of neuronal necrosis. These findings are discussed in relation to the postulated cellular organelle, the lysosome.