Praemia

Ohne Zusammenfassung

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Praemia

     

Transgenic rescue of defective Cd36 ameliorates insulin resistance in spontaneously hypertensive rats

Spontaneously hypertensive rats (SHR) display several features of the human insulin-resistance syndromes. Cd36 deficiency is genetically linked to insulin resistance in SHR. We show that transgenic expression of Cd36 in SHR ameliorates insulin resistance and lowers serum fatty acids. Our results provide direct evidence that Cd36 deficiency can promote defective insulin action and disordered fatty-acid metabolism in spontaneous hypertension.     

New views on RPE65 deficiency: the rod system is the source of vision in a mouse model of Leber congenital amaurosis

Leber congenital amaurosis (LCA) is the most serious form of the autosomal recessive childhood-onset retinal dystrophies. Mutations in the gene encoding RPE65, a protein vital for regeneration of the visual pigment rhodopsin in the retinal pigment epithelium, account for 10-15% of LCA cases. Whereas previous studies of RPE65 deficiency in both animal models and patients attributed remaining visual function to cones, we show here that light-evoked retinal responses in fact originate from rods. For this purpose, we selectively impaired either rod or cone function in Rpe65-/- mice by generating double- mutant mice with models of pure cone function (rhodopsin-deficient mice; Rho-/-) and pure rod function (cyclic nucleotide-gated channel alpha3-deficient mice; Cnga3-/-). The electroretinograms (ERGs) of Rpe65-/- and Rpe65-/-Cnga3-/- mice were almost identical, whereas there was no assessable response in Rpe65-/-Rho-/- mice. Thus, we conclude that the rod system is the source of vision in RPE65 deficiency. Furthermore, we found that lack of RPE65 enables rods to mimic cone function by responding under normally cone-isolating lighting conditions. We propose as a mechanism decreased rod sensitivity due to a reduction in rhodopsin content to less than 1%. In general, the dissection of pathophysiological processes in animal models through the introduction of additional, selective mutations is a promising concept in functional genetics.     

Intraaxonal iodate inhibits sodium inactivation

Zusammenfassung Iodat (IO ₃ ^– )-Ionen hemmen den Inaktivierungsvorgang des Natriumsystems, falls sie intraaxonal durch Diffusion vom abgeschnittenen Ende einer markhaltigen Froschnervenfaser her ans Innere der Schnürringmembran gelangen. Mit der Spannungsklemme erhält man dann in TEA-Ringer eine Strom-Spannungskurve des Natriumsystems auch mit lang dauernden Potentialänderungen. In der Stromklemme lassen sich unter diesen Umständen Aktionspotentiale mit Dauern bis zu 1 min registrieren.

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Dedicated to Prof. A. vonMuralt on the occasion of his 70th birthday.

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Sponsored by the Deutsche Forschungsgemeinschaft Sonderforschungsbereich 38 — Membranforschung.     

Ein neues Alkaloid aus dem Mycel einesClaviceps purpurea-Stammes. Zur Biogenese von Ergocristin

Summary A new alkaloid from the lyophilized mycelia of aClaviceps purpurea strain, N-[N-(d-Lysergyl)-l-valyl]-l-phenylalanyl-d-prolin-lactam, has been isolated and characterized. From its fast methanolysis it is deduced that the previously reported N-(d-Lysergyl)-l-valinmethylester is actually an artefact. The biogenetic significance and its possible role in biogenesis of Ergocristine is discussed.