Electroencephalographic activity (EEG) was recorded from the frontal cortex of unanaesthetized and urethane-anaesthetized lactating rats and analysed in relation to the pattern of milk ejection evoked by the nursing pups. The EEG of the anaesthetized rat fluctuated without experimental intervention between three distinctive patterns defined as synchronized, desychronized, and stage III activity, whilst reflex milk ejection recurred at intervals of about 6 min (range 2- greater than 20 min) throughout the 1-4 h period the pups were left attached to the nipples. For greater than 10 s before and for up to 60 s after each milk ejection, as judged from recordings of intramammary pressure and pup behaviour, the EEG was invariably synchronized throughout. Conversely, milk ejection (n greater than 300) was never observed during long periods of desynchronized, or stage III EEG activity. The vigorous increase in the sucking of the pups at milk ejection failed to produce a desynchronization (arousal) of the EEG as observed with other forms of sensory stimulation. Indeed, the sucking of the pups appeared to produce a soporific change i, the maternal EEG for spontaneous periods of desynchronization were not observed in the 30-60 min following the initial attachment of the pups to the nipples. Similar EEG patterns were seen in the unanaesthetized rat, though arousal from the synchronized state was more easily produced, e.g., by weak auditory signals. Milk ejection, as judged from the behaviour of the pups, recurred at intervals of 2 min or more during each 20-80 min period of nursing. The rat appeared somnolent for most of the nursing period and the EEG was always synchronized for greater than 10 s before each milk ejection (n greater than 200), though her eyes usually remained open. Arousal and desynchronization of the EEG was invariably observed in association with the increased pup behaviour at milk ejection. From these observations and the knowledge that oxytocin release from the neurohypophysis occurs about 10 s before milk ejection, we conclude that a synchronized EEG pattite for the expression of the milk-ejection reflex in the rat.

An inhibitor of aromatization, androsta-1,4,6-triene-3,17-dione (ATD), was administered to newborn male and female rats and various parameters of gonadal and sexual function were examined in adulthood. Males injected with 1 mg ATD on the day of birth (day 1) and on days 3, 5, 10 and 15 postnatally, subsequently (day 55) showed normal male and female copulatory behaviour, but were not able to maintain cyclicity in ovarian transplants. When the ATD was administered by Silastic implants, however, cyclicity in ovarian transplants did occur. Neither form of treatment brought about significant changes in neonatal plasma or testicular testosterone concentrations.Female rats implanted on day 3 of life with Silastic capsules containing ATD and then given an injection of 0\m=.\25 mg testosterone propionate on day 5 subsequently showed normal ovarian function, whereas the controls receiving only testosterone propionate showed persistent vaginal cornification, anovulation and polyfollicular ovaries.The results support the view that the central conversion of testicular androgens to oestrogens during the neonatal period is necessary to abolish cyclic gonadotrophin release and to suppress female copulatory behaviour.

Distribution and regulation of androgen receptor expression during fetal and neonatal virilization of the rat fetus was assessed by immunohistochemistry. In mesonephric duct derivatives the androgen receptor expression became evident first in the efferent ductules and epididymis (on fetal day 14), subsequently in the vas deferens and finally in the seminal vesicle. Mesenchymal cells of the urogenital tubercle were positive for androgen receptors from fetal day 14 onwards. In the mesenchymal cells of the prostate anlagen, androgen receptor positive cells were found first on fetal day 16. Administration of 5alpha-dihydrotestosterone to pregnant rats from day 11 to day 20 of gestation caused a stabilization of the wolffian duct in female fetuses. The androgen receptor expression pattern became similar as found in mail fetuses, and showed an increase in density and in frequency of androgen receptor positive cells. Administration of the androgen antagonist flutamide during the same interval caused a reduction in density and frequency of androgen receptor positive cells in male fetuses. These findings indicate that androgens enhance the expression of androgen receptors in the developing rat genital tract by induction of androgen receptor positive cells, and by increasing the frequency. The developmental pattern of androgen receptor expression in the rat mesonephric duct system reflects the androgen-responsiveness of the ducts, and is consistent with induction of the androgen receptor along the ducts by testosterone reaching these structures in an exocrine fashion.

No abstract

The present review aims to present a perspectiveon a relatively unknown part of the mammalian internal genitalia: their cranial suspensory apparatus. This apparatus shows wide divergence of development when examined during the fetal period or during adulthood, in males or females, or in individuals across a variety of species. In rats and other mamalian species the apparatus undergoes a distinct patern of sexually dimorphic development and fetal testicular androgens are proposed to play a key role in this process. Extensive development of this suspensory apparatus in females is argued to be a part of the anatomical adaptations of the genital apparatus to support the internal genitalia throughout pregnancy, including the relatively enormous growth towards the time of parturition. Minor development of this apparatus in males is judged to be a part of the anatomical requirements allowing developing testes to become displaced from the dorsal abdominal wall during the first stage of testicular descent. Extensive development of this suspensory apparatus in males generally seems to hinder testicular descent. Accordingly, the apparatus is well developed in so-called testicond species which do not show testis descent as a part of their normal male genital development. Furthermore, arguments are adduced that inappropriate and extensive development in species with testis descent may be a key aetiological factor in the disturbance of this process. Diagnosis and treatment of human cryptorchidism might profit from including an analysis of the development and function of (remnants of) the cranial testicular and epididymal suspensory apparatus.