Reduced number and altered morphology of microglial cells in colony stimulating factor-1-deficient osteopetrotic op/op mice.

The numerical density of microglial cells is reduced by 47% in the corpus callosum, by 37% in the parietal cortex and by 34% in the frontal cortex of mice mutant at the op locus which are totally devoid of colony stimulating factor-1 (CSF-1), the major growth factor for macrophages. Moreover, microglia in the frontal cortex of the op/op mice are smaller and have shorter cytoplasmic processes compared to control mice. Study suggests that CSF-1 plays a role in vivo in the formation and maturation of microglia and has little or no effect on perivascular cells.

Hyperplasia and hypertrophy of B cells in the islets of Langerhans in hamsters infected with the 139H strain of scrapie.

Previous studies showed that in hamsters the 139H, but not the 263K, scrapie strain caused a marked increase in pancreatic size and led to obesity, hypoglycaemia and striking hyperinsulinaemia. In the preceding paper (Ye et al., 1994), the islets of Langerhans in 139H-affected hamsters showed cellular atrophy, fibrosis, cytoplasmic vesicles and nuclear pathological changes. In the present study, the profiles of pancreatic islets were classified into three sizes with an image analyzer. The number and total area covered by "small" islet profiles were less in 139H-affected than in normal hamsters. In contrast, the number and the area of "medium" and "large" islet profiles were significantly greater in 139H than in normal hamsters. With antibodies to insulin, glucagon, somatostatin and pancreatic polypeptide, the proportions of B, A, D and F cells were determined. With somatostatin-positive cells arbitrarily given a value of 1, the ratio of B:A:D:F cells in the islets was 27:5:1:0.04 in normal hamsters and 122:7:1:0.04 in 139H-affected hamsters. The increase in B cells would account for the islet enlargement and the hypoglycaemia-hyperinsulinaemia seen in 139H-affected hamsters.

Effect of infection with the 139H scrapie strain on the number, area and/or location of hypothalamic CRF- and VP-immunostained neurons.

Scrapie is a transmissible neurodegenerative disease which shares some characteristics with Alzheimer disease (AD). Recent studies show abnormal enlargement of the adrenal glands and kidneys in 139H-affected hamsters. Using immunocytochemical techniques with antibodies to corticotropin-releasing factor (CRF) and vasopressin (VP), we observed the following: (1) a significantly higher number of CRF-immunostained neurons in the preoptic nucleus of hypothalamus of 139H-affected hamsters than controls; (2) the area of VP-immunostained (ir-VP) neurons in the lateral hypothalamus, which includes the internuclear group of magnocellular neurons and the nucleus circularis, was significantly lower for 139H-affected hamsters than for controls; and (3) no significant difference between 139H-affected and control hamsters with regard to the number of ir-VP neurons in the dorsal-medial hypothalamus (DMH), including the paraventricular hypothalamus, or the supraoptic nuclei. However, the population of ir-VP neurons in the DMH shifted to the anterior part of the hypothalamus in 139H-affected hamsters. Three-dimensional models of the immunostaining were prepared and these provide clear depictions of the changes noted. The changes in the CRF and VP systems in 139H-affected hamsters suggest that the neuroendocrine system can be affected by unconventional slow infections.