PubMed Health⌕ Search

Biomedical subjects

V L Friedrich

Publications and source records attributed to V L Friedrich.

59 records · Page 4Linked to original sources
PubMed1975

Hyperplasia of oligodendrocytes in quaking mice.

The number of neuroglial cells in selected fiber tracts of 90-day-old quaking and normal mice was determined by a combination of light and electron microscopy. Oligodendrocytes of quaking mice are normal in number in the anterior commissure and corticospinal tract (in the cervical spinal cord) but are increased two- to fourfold in the optic nerve and the fasciculi cuneatus and gracilis (in the cervical spinal cord). The nuclei and perikarya are normal in size or smaller than normal. Those tracts with the greatest hyperplasia of oligodendrocytes also have the greatest content of myelin, suggesting that cell number influences content of myelin. However, the volume of myelin per oligodendrocyte also varies, between 2 and 11% of normal, in the different tracts of the mutant. The hyperplasia of oligodendrocytes in quaking mice may arise as compensation for their decreased production of myelin and reflect a normal plasticity in the processes of myelination. If so, the mutant may be a useful system for study of the regulation of myelogenesis.

Animals↗
PubMed1975

[Time of onset and regression of D-penicillamine activity, measured by rupture load of rat skin].

Two experiments were carried out to determine the period of time for a) the decrease of the load resulting in rupture of excised dorsal skin strips of the rat induced by daily oral treatment with D-beta, beta-dimethylcysteine (D-penicillamine, Metalcaptase) and b) the effect produced by D-penicillamine treatment to subside after discontinuation of the substance. 1. On the 5th day of treatment (320 mg/kg/day), the load resulting in rupture of excised dorsal skin strips of rats from an animal group decreased from 3480 p (initial value) to 2350 p. On the 9th day of treatment, the value for the load resulting in rupture dropped to 1790 p. Further decrease of the load resulting in rupture cannot be obtained even after a 2 weeks' treatment with 320 mg/kg D-penicillamine. 2. An animal group was treated with 320 mg/kg D-penicillamine for 7 days. At the end of this period of treatment, the load resulting in rupture of excised dorsal skin strips amounts to 1400 p. After discontinuation of the medication, the load resulting in rupture of the dorsal skin is determined at intervals of several days. 6 days after discontinuation of the test substance, a marked rise was observed and after 15 days, no difference was found between the initial value of non-treated animals and previously treated animals. Thus, it takes a few days only to induce a decrease of the load resulting in rupture by D-penicillamine and its recovery after discontinuing the medication.

Administration, Oral↗
PubMedDate not supplied

Restricted migration of transplanted oligodendrocytes or their progenitors, revealed by transgenic marker M beta P.

Transgenic mice of line M beta P3 express bacterial beta-galactosidase in oligodendrocytes but not other cells of the CNS. The marker enzyme, demonstrated histochemically or by immunostaining in oligodendrocyte cell bodies and along myelin internodes, appears at the time of myelination and persists thereafter; in transplantation experiments, the marker may serve to indicate both the source of particular cells and their state of differentiation. The subventricular zone of the lateral ventricle, grafted from transgenic to wild-type perinatal recipient mice, yields histochemically labeled oligodendrocytes in surrounding host tissue. When grafts are placed in cerebral cortex near callosal radiations, graft-derived oligodendrocytes are found in cerebral cortex and subcortical white matter as far as 1.5 mm from the site of implant but not in nearby caudoputamen. This study is the first to document differentiation of transplant-derived oligodendrocytes in normal developing CNS. Our results are consistent with the well-established notion that oligodendrocyte progenitors migrate during normal development and suggest that such migration might be guided or restricted by mechanisms yet to be identified.

Animals↗