Purification of a non-dopaminergic and non-GABAergic prolactin release-inhibiting factor (PIF) in sheep stalk-median eminence

Prolactin release-inhibiting factor (PIF) extracted from 1200 sheep stalk-median eminences was purified by gel filtration on a Sephadex G-25 column (4.5 X 150 cm). PIF activity was determined by measuring the inhibition of prolactin release from dispersed anterior pituitary cells of adult male or estrogen-primed, ovariectomized rats. Using this system, PIF was detected in tube fractions 122-127 (volume = 20 ml/tube). These fractions also contained LHRH and somatostatin; however, these peptides had no prolactin-inhibiting activity in the quantities present. No dopamine or gamma-aminobutyric acid (GABA) was detected in the active fractions by radioenzymatic assay and fluorophotoenzymatic assay, respectively. Furthermore, receptor blockers for dopamine or GABA did not interfere with the PIF activity. These findings indicate that the PIF activity cannot be attributed to either dopamine or GABA, both of which are known to inhibit prolactin release, and provide evidence for the presence of a non-dopaminergic and non-GABAergic PIF within the hypothalamus.     

Biosynthesis of Ubiquinone in Escherichia coli K-12: Location of Genes Affecting the Metabolism of 3-Octaprenyl-4-hydroxybenzoic Acid and 2-Octaprenylphenol

Two genes (ubiB and ubiD) concerned with two successive reactions in ubiquinone biosynthesis in Escherichia coli were mapped and found to be closely linked. Mutant strains of E. coli carrying the ubiB(-) and ubiD(-) alleles were shown to accumulate 2-octaprenylphenol and 3-octaprenyl-4-hydroxybenzoic acid, respectively. These compounds were isolated and identified by using nuclear magnetic resonance and mass and infrared spectroscopy. Cell extracts from the mutant strain carrying the ubiD(-) allele lack 3-octaprenyl-4-hydroxybenzoate decarboxylase activity.     

Methyl Green as a Cartilag Setain; Human Embryos

The development of this technique derived from a need to demonstrate the sites of developing cartilage in the human embryo. The basic procedure was that of Yntema (1970), which used methyl green on turtle embryos. However, the thickness of the soft tissues in human embryos of 90-125 mm crown-rump (CR) length and the opacity caused by pigments in this tissue when the specimen was cleared necessitated the modification of the original procedure; specifically, the introduction of bleaching. The altered procedure is given below.     

Plasmodium berghei: inhibitors of ornithine decarboxylase block exoerythrocytic schizogony

DL-alpha-difluoromethylornithine and DL-alpha-monofluoromethyldehydroornithine methyl ester, inhibitors of ornithine decarboxylase, blocked exoerythrocytic schizogony of Plasmodium berghei in mice and in cultured human hepatoma cells. These effects were reversed by exogenous administration of the polyamine, spermidine. The antimalarial drug, primaquine, the side chain of which is structurally analogous to a natural polyamine, did not enhance the activity of alpha-difluoromethylornithine or alpha-monofluoromethyldehydroornithine methyl ester. These results extend previous observations that polyamines influence the malaria parasite's schizogony outside the red blood cell but not within it.     

Evidence for hormonal participation in the natriuretic and kaliuretic responses to intraventricular hypertonic saline and norepinephrine.

To examine if hypothalamic or pituitary hormones are involved in the induction of the natriuresis which follows the injection of hypertonic saline or norepinephrine into the third ventricle, lesions were placed in the median eminence and the responses to intraventricular norepinephrine or hypertonic saline were evaluated. Sham lesions in which the electrode was lowered into the brain but stopped short of the hypothalamic region did not interfere with the natriuresis, kaliuresis, and antidiuresis induced by the third ventricular injection of either hypertonic sodium chloride or norepinephrine. Lesions in the median eminence which induced diabetes insipidus as evidenced by an increase in water consumption to approximately four times normal completely abolished the natriuresis and kaliuresis in response to intraventricular hypertonic saline or norepinephrine and diminished the antidiuresis. The observations suggest the possibility that a natriuretic hormone(s) is involved in the induction of central natriuresis.     

Cholecystokinin antagonist,proglumide, stimulates growth hormone release in the rat

Previous studies have revealed a stimulatory action of cholecystokinin on growth hormone release in the rat. To evaluate the physiologic significance of these effects we employed the cholecystokinin antagonist, proglumide and injected it intravenously and intraventricularly (third cerebral ventricle, 3V) to determine its actions on growth hormone. The experiments were performed in conscious, freely moving rats with indwelling cannulae in the 3V and/or external jugular vein. Intraventricular injection of 2 or 10 □g of proglumide significantly elevated plasma growth hormone concentrations in intact and castrated male rats and in ovariectomized females. Intravenous injections of 10 or 100 □g of proglumide were also effective in elevating growth hormone in a dose-related manner. Surprisingly, the response to the lower dose given intraventricularly was somewhat greater than that of the higher dose. We speculate that these stimulatory effects of proglumide given intraventricularly are due to the agonist action of proglumide at these doses since action of cholecystokinin itself is to increase plasma growth hormone following its intraventricular injection. The studies therefore do not establish a physiologically significant growth hormone-releasing action of brain cholecystokinin but provide more evidence that activation of cholecystokinin receptors in the brain can induce a stimulation of growth hormone release either by activation of the release of growth hormone-releasing hormone or by inhibition of the release of somatostatin or by a combination of these two actions.