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Quantitative morphological analysis of the cerebellar nuclei in normal and lurcher mutant mice. I. Morphology and cell number.

The present study indicates that the cerebellar nuclei of the mouse are essentially identical in structure with those described in the rat, and that the atrophic cerebellar nuclei in lurcher mutant mice exhibit a comparable anatomical organization. A quantitative estimate of the atrophy observed in the cerebellar nuclei of the adult lurcher mutant mouse reveals an overall 60% decrease in volume. Cell counts in the wild-type cerebellar nuclei reveal a total of 8,528 principal neurons and 10,203 small neurons. The ratio of small/principal neurons is 0.5 in the fastigial nucleus and between 1 and 1.5 in other subdivisions. In lurcher, the principal neurons are slightly reduced in number (-20%) in the nuclear complex, while the population of small neurons is reduced by 37% in the interposed and dentate nuclei, but is unchanged in the fastigial nucleus. These results suggest that the massive deafferentation of the cerebellar nuclei that occurs between 10 and 30 days of age in lurcher mutants has a relatively mild effect on the principal cerebellar nuclear neurons. In the population of small neurons, however, the effect of deafferentation may be exacerbated by a secondary retrograde transneuronal degeneration brought on by the severe degeneration of inferior olivary neurons and cerebellar cortex in this mutant.

Animals↗

The secretory ameloblast of the mini-pig foetus: Morphology, and effect on morphology of various aldehydes and of delayed fixation.

Electron microscopic investigations of secretory ameloblasts from deciduous tooth germs of mini-pig foetuses and investigations of the ability of various fixatives to preserve these cells in tooth germs immersion-fixed in to 5 min, 10 min, 15 min, 20 min and 40 min after death of the mother gave the following results: 1. The ameloblasts exhibit ultrastructural characteristics typical of exocrine secretory cells of merocrine type. 2. The localization of organelles is as in rodent secretory ameloblasts, but differs from the location in the human analogues. 3. Fixation with 4% formaldehyde invariably gives unacceptable ameloblast preservation. 4. Fixation with 2.5% glutaraldehyde gives fair preservation of the ameloblasts when the germs are fixed within 10 min of the death of the mother. 5. Fixation with a fixative mixture 2% formaldehyde-1.25% glutaraldehyde gives good preservation when the ameloblasts are fixed within 15 min of the death of the mother. 6. Fixation with a fixative mixture 2% formaldehyde-1% glutaraldehyde-1% acrolein gives good ameloblast preservation when the germs are fixed within 15 min of the death of the mother.

Acrolein↗

Morphology of the epididymis of the cock (Gallus domesticus) and its effect upon the steroid sex hormone synthesis. I. Ontogenesis, morphology and distribution of the epididymis.

The epididymis of the cock is divided into a main part and an appendix epididymidis. The main part of the epididymis is firmly connected to the testis. The sperm transporting tubes open into the ductus epididymidis along its entire length. The rete testis, as the most proximal part of the epididymis, develops from mesenchym cells. The rete testis connects the tubuli seminiferi with the ductuli efferentes proximales which develop from the Bowman's capsules of the mesonephros. The ductuli efferentes distales develop from the proximal tubules, conducting segments (loops of Henle), and the distal tubules of the mesonephros. The short ductuli conjugentes which open into the ductus epididymidis, originate from the connecting segments of the mesonephros. In the sexually mature cock the rete testis, the ductuli efferentes proximales, and the ductus epididymidis all show an enlargement in the lumen. In the ductuli efferentes proximales and in the ductus epididymidis one can observe a formation of globuli and cell protrusion which lead to a loss of the surface structure of the epithelial cells. The appendix epididymidis and the capsula fibrosa of the adrenal gland are joined by connective tissue. The appendix epididymidis consists of the blindly ending ductus aberrans (the crainal continuation of the ductus epididymidis) and the ductuli aberrantes which open into the ductus aberrans. The blind ends of the ductuli aberrantes end in the capsula fibrosa of the adrenal gland.

Animals↗

The Mayer-Rokitansky-Küster syndrome. An analysis of its morphology and embryology. Part I: Morphology.

The histological appearance of the rudimentary uterus, endometrium, uterine tube, Gartner's duct, round ligament, vagina and ovary is described in ten case of the MRK syndrome. When the layout of the pelvic contents of patients with this syndrome is compared with that of a normal embryo of 20 mm CRL (stage 20), the following conclusions may be drawn. The MRK syndrome can be regarded as resulting from the cessation of development of the Müllerian duct, which in this condition extends only as far as its attachment to the caudal mesonephric ligament, the round ligament. The adjacent structures beyond this point, which include the connecting strand and smooth muscle bundles dorsal to the bladder and vaginal rudiment, are derivatives of the Wolffian duct or Gartner's duct respectively. Our findings suggest that this syndrome is due to a deficiency of the estrogen and gestagen receptors. This deficiency may inhibit the further development of the embryonic Müllerian duct and account for the subsequent faulty differentiation of its existing elements. It is still undecided why, in cases of the MRK syndrome, development of the Müllerian duct ceases at the attachment of the caudal mesonephric ligament (later the round ligament). Further research is necessary to answer this question.

Adolescent↗

Morphologic observations in a case of lethal variant (type I) metatropic dysplasia with atypical features: morphology of lethal metatropic dysplasia.

Metatropic dysplasia accounts for approximately 5% of cases recorded by the International Skeletal Dysplasia Registry, with a single recorded lethal case. Four forms of the disease are currently recognized: type I, lethal autosomal recessive form; type II, nonlethal autosomal recessive form with survival to childhood; type III, autosomal dominant form with typical features, and type IV, a mild form with uncertain inheritance. The literature contains few well-documented reports of the histopathologic findings in metatropic dysplasia. In this report, we present the radiologic and histopathologic features in a cas e of type I metatropic dysplasia, with the unusual features of a persist ent tail, unique lung dysmorphology, and thyroidal agenesis.

Abnormalities, Multiple↗