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Macrophages of endocrine organs have been identified by immunohistochemical localization of the macro- The mononuclear phagocyte system is a group of cells that consists of bone marrow precursors, blood monocytes, and tissue macrophages (1). F4/80, a 160-kilodalton membrane glycoprotein antigen defined by a rat monoclonal antibody, is a marker for mouse mononuclear phagocytes in vitro (2, 3) and in vivo (4-7). The present paper is concerned with immunohistochemical localization of the macrophage marker F4/80 in endocrine organs of the mouse. METHODSThe animals used in this study were adults between 10 and 14 weeks of age. Females used in the study of the ovary were maintained in a lighting regime of 14 hr light, 10 hr dark and were chosen after displaying two consecutive 4-day estrus cycles as defined by daily vaginal smearing. The animals were perfused through the left ventricle with heparinized saline followed by 0.5% glutaraldehyde in 1% sucrose/0.1 M sodium cacodylate as described (4). It was noted that the reliability of this method, particularly for endocrine organs, was increased if the preperfusion buffer (heparinized saline) was warmed to 37°C. Fixed tissues were excised, dehydrated through ethanol, then 100% isopropyl alcohol, cleared in ligroin (BDH), and embedded under reduced pressure in Polywax (57°C melting point, Difco). Alternatively, tissues were embedded in low-melting-point 42°C RAL paraffin wax (Stansen Scientific, Sydney, Australia), which gave slightly poorer morphology but more reliable antigen preservation. This alternative was used for testis and pancreas.

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Mutations in animals have provided insight into many aspects of normal and pathological human physiology. This paper reports the discovery and initial characterization of a new mutant dwarf rat. The mutation, inherited as an autosomal recessive, arose spontaneously in a breeding colony of Lewis rats at the Medical Research Council Cellular Immunology Unit, Sir William Dunn School of Pathology, Oxford, U.K., in 1985 and the strain has now been established both in Oxford and at Mill Hill. Body growth in the mutant is retarded such that at 3 months of age both males and females weigh approximately 40% less than their normal litter-mates, and continue to grow at a slower rate. The mutants show a selective reduction in pituitary GH synthesis and storage (pituitary GH concentrations were approximately 10% of normal in males and 6% in females). The concentration of their anterior pituitary trophic hormones (LH, TSH, prolactin and ACTH) were within the normal range in dwarf animals. Exogenous GH treatment for 5 days resulted in an increase in growth rate from 1.5 +/- 0.3 to 3.9 +/- 0.4 g/day in male mutants, and 0.8 +/- 0.2 to 3.1 +/- 0.1 g/day in females. Longitudinal bone growth rates were more than doubled by this treatment from 49 +/- 5 to 100 +/- 10 micron/day in females and from 52 +/- 11 to 131 +/- 16 micron/day in males. Dot blot and Northern blot analysis of pituitary mRNA extracts revealed that the GH message in mutants was between 20 and 25% of normal, and that the GH transcript was of normal size.(ABSTRACT TRUNCATED AT 250 WORDS)

The roles of FSH and androgen in the postnatal development of Sertoli cell number and function have been investigated using mice that lack FSH (FSHbetaKO), FSH-receptors (FSHRKO), or androgen receptors (Tfm). At birth and d 5, Sertoli cell number was normal in FSHRKO and FSHbetaKO mice, but was significantly reduced on d 20 and in adulthood. In contrast, Sertoli cell number was reduced at birth in Tfm mice and remained significantly less than normal up to adulthood. Sertoli cell activity was determined through measurement of 11 different mRNA transcript levels. From birth to adulthood, the expression of most transcripts increased, with a significant rise occurring between d 5 and 10. In animals lacking FSH stimulation, mRNA expression (measured per Sertoli cell) was largely normal on d 5, but was reduced in seven transcripts on d 20 and in five transcripts at adulthood. In Tfm mice two transcripts showed reduced expression on d 5, and four were reduced on d 20, although expression in adult Tfm mice did not differ from that in normal cryptorchid controls. The results show that 1) testosterone, but not FSH, is required for Sertoli cell proliferation during fetal and early neonatal life; 2) FSH and testosterone both regulate the late stages of Sertoli cell proliferation; 3) FSH has a general trophic effect on Sertoli cell activity in the pubertal and adult mouse; and 4) androgens are required for specific transcript expression during prepubertal development. Specific effects of androgens were not seen in the adult, although these may be masked by the effects of cryptorchidism.