[Ragged--a new rexoid mutant rat with large sebaceous gland].

A new hair defected mutant rat was established. This mutant was covered with ragged hair since about 10 days of age, then transiently lost most of hair in the back at approximately 5 weeks of age and re-covered with ragged hair thereafter. Thickened eyerids occurred since about 3 weeks of age. Histological examination revealed enlarged sebaceous glands with greater number of sebaceous cells in the back skin. The oil stained skin samples showed normal sebaceous transformation and pilosebaceous canal. Genetical analysis showed that the ragged hair character was a single recessive trait and indicated that this single recessive gene was not linked with the coat color genes, non-agouti (a), albino (c) and hooded (h). From the present data and previous reports, we recommended this single recessive gene is a new rexoid mutation thereby we termed this gene "Ragged (rg)".

Suprainguinal ectopic scrota of TS inbred rats.

A new rat line (TS inbred rats) showing uni- or bilateral ectopic scrota in about 70% of the males was established. Ectopic scrota were elongated pouches of the thin muscle layer under the suprainguinal body skin, in which hypoplastic testes and epididymides were seen. Genetic analysis revealed that the ectopic scrotum was controlled by multiple genes. Groups of 5 normal, uni- and bilaterally affected rats were killed at 25 weeks of age. Histologically, ectopic testes of uni- and bilaterally affected rats showed arrest of spermatogenesis at the primary spermatocyte stage. Contralateral testes of unilaterally affected rats were normally descended and showed normal spermatogenesis. No abnormality was seen in the urinary system. Plasma concentrations of FSH were significantly elevated in bilaterally affected rats but plasma concentrations of testosterone and LH were unchanged in uni- and bilaterally affected rats. Pituitary contents of LH and FSH were significantly elevated in bilaterally affected rats. The endocrinological status of TS inbred rats was therefore similar to that of experimentally induced cryptorchid rats.

A new male pseudohermaphrodite rat mutant with androgen deficiency.

A male pseudohermaphrodite rat mutant showing a blind-ending vagina, small undescended testes, rudimentary male sex accessory organs and XY karyotype was investigated. Genetic analysis revealed an autosomal single recessive transmission of this defect and indicated that the gene action is restricted to males. Microscopic examination showed an absence of typical Leydig cells in testes of the mutant. Plasma concentrations of testosterone were extremely low and the values were comparable to those of castrated male rats and did not change after castration and/or after administration of hCG. Plasma concentrations of LH and FSH were remarkably high and the values were comparable to those of long-term castrated normal male rats which declined to basal levels after administration of exogenous testosterone. Weights of thymus and adrenal glands decreased and weights of preputial glands, kidneys and male accessory sex organs increased in response to exogenous testosterone. These results indicate that the primary defect in the mutant is an androgen deficiency probably due to a Leydig cell agenesis in the testes.

Sperm retention cysts in the efferent duct and testicular atrophy of TE inbred rats.

Sperm retention cysts were observed in the efferent duct of TE inbred rats at 15 weeks of age. Spermatozoa agglutinated in the efferent duct with destruction of the epithelium. Testicular weight increased or decreased. Diameter of the seminiferous tubules was enlarged in testes that increased in weight and germinal cells degenerated in the atrophied testes. After 30 weeks of age, the tubules of the efferent duct were sometimes replaced by scars and testicular atrophy became more frequent. In 3 out of 5 normal rats united by parabiosis with TE males for 25-27 days, cysts occurred in the efferent duct.

[Morphological study on the hypoplastic testis with aplasia of the epididymis, ductus deferens, and gland of the ductus deferens in the TW inbred rat].

In the TW inbred rat, about 50% of the males show bilateral or unilateral testicular hypoplasia with aplasia of the ipsilateral epididymis, ductus deferens and gland of the ductus deferens. To investigate the pathogenesis of the testicular abnormality in the TW rats, the weight and morphology of the testes on the aplastic and normal side were studied between one week and one year of age. The weight of the testes on the affected side was greater than those on the normal side at four and five weeks. However, it rose to a plateau at six weeks and then remained at about one half to one third the weight of a normal testis. As for the testicular histology, there were no obvious changes from one day to three weeks of age. The diameter of the seminiferous tubules became larger and the number of germ cells decreased at four and five weeks. At six weeks, degeneration and loss of germ cells were observed and many multinucleated giant cells appeared. Thereafter, the loss of germ cells became more severe, and they eventually disappeared with increasing age, but Sertoli's cells continued to exist. In the interstitial area, edematous changes and proliferation of Leydig's cells were observed. The efferent duct of another strain, with normal testes, was ligated at three weeks of age, and changes of the testis after the operation were examined to investigate whether or not these anomalies of the TW strain were due to the absence of the accessories, which may block the excretion of the testicular fluid.(ABSTRACT TRUNCATED AT 250 WORDS)