Selective loss of Purkinje cells from the rat cerebellum caused by acrylamide and the responses of beta-glucuronidase and beta-galactosidase.

Abstract

Acrylamide (30 mg/kg) given daily to rats five times each week for 3 weeks leads to progressive loss of Purkinje cells. The necrotic cells begin to be visible from the third day and their numbers reach a peak at the time when the dosing ceases at 18 days. They are less frequent thereafter, but are still visible almost 3 weeks later in small numbers. The density of Purkinje cells per millimeter falls to about 70% of normal at the 7th day, and a similar degree of reduction of the neuronal marker enzyme, beta-galactosidase, is found over the same time scale. By contrast, while there is a brisk macrophage/microglial response in the molecular layer to the loss of the Purkinje cell dendrites, the increase in beta-glucuronidase activity is relatively minor and is not significantly different from normal until after the 21st day. These responses are discussed in the context of the use of lysosomal enzyme activities in the assay of certain neurotoxic lesions.