Progenitor cell maintenance requires numb and numblike during mouse neurogenesis

Neurons in most regions of the mammalian nervous system are generated over an extended period of time during development. Maintaining sufficient numbers of progenitors over the course of neurogenesis is essential to ensure that neural cells are produced in correct numbers and diverse types. The underlying molecular mechanisms, like those governing stem-cell self-renewal in general, remain poorly understood. We report here that mouse numb and numblike (Nbl), two highly conserved homologues of Drosophila numb, play redundant but critical roles in maintaining neural progenitor cells during embryogenesis, by allowing their progenies to choose progenitor over neuronal fates. In Nbl mutant embryos also conditionally mutant for mouse numb in the nervous system, early neurons emerge in the expected spatial and temporal pattern, but at the expense of progenitor cells, leading to a nearly complete depletion of dividing cells shortly after the onset of neurogenesis. Our findings show that a shared molecular mechanism, with mouse Numb and Nbl as key components, governs the self-renewal of all neural progenitor cells, regardless of their lineage or regional identities.     

Membrane potential measurement in mouse salivary gland cells

Zusammenfassung Acetylcholin erzeugt auf das Membranpotential von Azinuszellen der Glandula submandibularis der Maus eine diphasische Veränderung des Membranpotentials (rasche Hyperpolarisation und langsame, verzögerte Depolarisation oder rasche Depolarisation und langsame Hyperpolarisation). Hinweise sprechen dafür, dass Acetylcholin die Permeabilität für Na⁺-und K⁺-Ionen erhöht.

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I am grateful to Dr.E. K. Matthews, who placed all necessary facilities in his laboratory at my disposal, for his great interest in this project and for many useful discussions.

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The excellent technical assistance ofG. L. Pedersen is gratefully acknowledged. Financial support came from; the Carlsberg Foundation, The Wellcome Trust and Johann and Hanne Weiman's legacy.     

Impaired amylase release from the parotid gland of rats treated with reserpine

Summary Using an automated system for the analysis of amylase, the release of this enzyme was compared in superfused parotid gland segments from control and reserpine treated rats. Stimulant-evoked amylase release was delayed and of smaller magnitude in the glands of the treated animals and a reduction of the transmembrane K⁺ gradient caused a smaller and short lasting reduction in Ach-evoked release of amylase in the glands from these animals.This work was supported by grants from the Cystic Fibrosis Research Trust (U.K.), Cystic Fibrosis Foundation (USA) and University of Missouri.     

Transmembrane secretory potentials in the cat submandibular gland during perfusion with potassium-free and low sodium Locke solutions

Zusammenfassung Während der Perfusion der Submandibulardrüse der Katze mit kaliumfreier Lockelösung oder mit einer Lockelösung, in der das meiste Kochsalz durch Tetraethylammoniumchlorid ersetzt wurde, sind die sekretorischen Potentialdifferenzen der basalen Azinuszellmembran vergrössert. Ein Kaliumstrom aus der Azinuszelle, der teilweise von einem Natriumstrom in die Zelle kurzgeschlossen wird, könnte die sekretorischen Potentialdifferenzen erklären.

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With the technical assistance of G.Pedersen.     

N″-cyano-N-4-pyridyl-N′-1,2,2-trimethylpropylguanidine,monohydrate (P 1134): A new,potent vasodilator

Summary N-cyano-N-4-pyridyl-N-1,2,2-trimethylpropylguanidine, monohydrate (P 1134) is a new agent which induces a marked and sustained hypotensive response in normotensive and renal, neurogenic, and spontaneously hypertensive rats, as well as in normotensive and renal hypertensive dogs. The overall potency of this compound is 2–3 times greater than that of hydralazine. The fall of blood pressure is accompanied by an increase in heart rate and cardiac output and a decrease in total peripheral resistance. The hypotensive effect appears to be due primarily to a direct relaxant effect on vascular smooth muscle.Acknowledgment. The helpful comments and advice of Dr W.O. Godtfredsen are greatefully acknowledged.