Different effects of K+ and Ca++ on alpha-MSH and ACTH release from superfused neurointermediate lobe of the rat hypophysis.

The effects of K+-enhanced and Ca++-free media on alpha-MSH and adrenocorticotropic hormone (ACTH) release from superfused neurointermediate lobe (NIL) were studied in the same experiments. High K+ caused reversible and repeatable inhibition of alpha-MSH release and stimulation of ACTH release, Removal of Ca++ impaired the effect of K+, irreversibly for alpha-MSH and reversibly for ACTH. The existence of both melanotrophic and corticotrophic cells within the intermediate lobe (IL) of rat hypophysis could account for the different effects of ionic modifications on in vitro alpha-MSH and ACTH release.

Estradiol and progesterone binding in rabbit placenta during gestation.

In rabbit fetal placenta, 17 beta-estradiol and progesterone are not bound by specific (high affinity, low capacity) components in the cytosol, in spite of the fact that this part of the organ is very reactive to modifications in hormonal conditions. Cytosol receptors for estradiol and progesterone are found only in the maternal part of the placenta; apparent association constants are about 3 X 10(8) M-1 for 17 beta-estradiol and about 2 X 10(8) M-1 for progesterone (in the absence of glycerol) at 4 degrees C. Estradiol is also bound to nuclei in cells of the maternal placenta in vivo and in vitro. Concentrations of estradiol and progesterone binding sites show marked variations during normal gestation in the rabbit. For estradiol the number of binding sites increases from day 10 to day 14, then decreases until parturition. This number increases for progesterone from day 10 to day 16, then decreases until day 27.

[Placental and fetal growth in the rabbit: influence and mechanism of action of ovarian hormones (author's transl)]. / Croissance placentaire et foetale chez la lapine: influence et mode d'action des hormones ovariennes.

During the second half of gestation in normal rabbits, hormonal overdoses result in similar modifications of placental and fetal weights, as in castrated animals identically treated (fig. 1). Nucleic acid and protein assays show that hormonal mechanisms are very different for the maternal (table I) and fetal portions of the placenta (table II): progesterone alone promotes a hypertrophy of the fetal placenta and hyperplasia of the maternal placenta. Estradiol at physiological levels counteracts these effects. Moreover, progesterone (fig. 3) and estradiol (fig. 2) receptors are found only in the maternal placenta, although the fetal placental is the most sensitive to the hormonal environment.

Colchicine effects on neurosecretory neurons and other hypothalamic and hypophysial cells, with special reference to changes in the cytoplasmic membranes.

The morphological effects of colchicine on the entire neurosecretory (NS) tract and on various hypothalamic nuclei have been studied. The perturbations in axonal flow, indicated by the accumulation of NS material, coincide with fragmentation of the cytoplasmic membranes, i.e. the Golgi apparatus and the endoplasmic reticulum, whereas the neurotubules remain relatively well preserved. Autophagic destruction of NS material is observed along the entire length of the NS fibres. The rapid and systematic changes in the axoplasmic reticulum, known to store calcium, lead us to envisage a role for this system-similar to that of the sarcoplasmic reticulum-in controlling the transport of NS vesicles. The junctional zone between the stalk and the neural lobe seems to play a particular role in the transport of NS material to the posthypophysial terminals of the NS axons. Colchicine provokes an increase in dense-cored vesicles in most of the neurons of the other hypothalamic nuclei studied: arcuate, suprachiasmatic, periventricular and ventromedial. Membranous alterations are also observed in these sites. Colchicine administered to animals which were hypothyroid, castrated or adrenalectomized, reveals stimulated neurons, identified by their excessive content of dense-cored vesicles. These neurons display no specific localization, for they occur in all hypothalamic nuclei, irrespective of the stimulation. The frequency of stimulation of neurons of the periventricular nucleus is striking.

Subcellular localization of calcium in the mouse hypophysis. I. Calcium distribution in the adeno- and neurohypophysis under normal conditions.

Application of the K-pyroantimonate technique combined with glutaraldehydeosmium fixation results in a reproducible intracellular distribution of mineral precipitates in the mouse hypophysis. Control experiments--with chelators and electron probe microanalysis--reveal that these precipitates consist mainly of calcium. Regularly present in the mitochondria, Ca also seems to be stored in the Golgi apparatus of the glandular cells and in the axoplasmic reticulum and the "synaptic" vesicles of the neurosecretory fibres. These structures thus appear able to control intracytoplasmic calcium movements. These observations agree with physiological data showing the existence of an intracellular Ca pool that can be mobilized by specific stimulation. The presence of diffuse precipitates in the pituicytes, together with the existence of gap junctions between them, suggest that these cells regulate the ionic environment of the neurosecretory nerve fibres; in this way, they too might participate in neurohypophysial hormonal release.