The effect of injury on two hydrolases in the hypoglossal nucleus, with quantitative data on N-acetyl-beta-glucosaminidase.

N-acetyl-beta-glucosaminidase and acid phosphatase were studied histochemically in sections of hypoglossal nuclei of normal adult male albino rats, and rats from 1 to 56 days after axotomy of the left hypoglossal nerve, or after injection of botulinum toxin into the left side of the tongue. Both axotomy and botulinum caused a diminution of neurone perikaryal glucosaminidase reaction product on the operated side, but an increase of reaction product elsewhere in the operated nucleus. Whereas the effect of axotomy lasted from 5 to 42 days post-operatively, that of botulinum ceased between 28 and 42 days. Axotomy and botulinum both caused an increase of neuronal acid phosphatase (after a short incubation time) from 2 to 21 days post-operatively in injured nuclei. Glucosaminidase reaction product measured microdensitometrically in isolated cells showed a statistically significant diminution in injured neurones at 18 days after axotomy. There was no change in the amount of reaction product per cell in pericytes, astrocytes, or non-astrocyte glia. Sections scanned quantitatively showed that normal and operated nuclei had a similar amount of reaction product, thus the neuronal diminution must be balanced by the increase elsewhere, either in the elevated numbers of non-astrocyte glia, or in the neuropil.