Weitere Versuche über binokulare Mischung von Spektralfarben

Zusammenfassung Mit einem neuen nach meinen Angaben gebauten Apparat (Schmidt & Haensch, Berlin) zur binokularen Farbenmischung, der quantitative Bestimmungen unter Verwendung von Vergleichslichtern gestattet, werden die früher von mir gewonnenen Ergebnisse bestätigt und erweitert. Bei Gelbgleichungen sowie Purpurgleichungen ist die binokular vom kurzwelligen Licht nötige Menge geringer, wie monokular. Bei Weißmischungen, bei welchen das langwellige Licht von immer kürzerer Wellenlänge genommen wird, zeigt sich zunächst dasselbe Verhalten; dann aber schlägt nach Durchgehen durch einen Gleichheitspunkt das Mengenverhältnis in das Gegenteil um, indem nun binokular mehr kurzwelliges Licht nötig ist, wie monokular.     

Modulation of (3)H-noradrenaline release by presynaptic opioid, cannabinoid and bradykinin receptors and beta-adrenoceptors in mouse tissues

Release-modulating opioid and cannabinoid (CB) receptors, beta-adrenoceptors and bradykinin receptors at noradrenergic axons were studied in mouse tissues (occipito-parietal cortex, heart atria, vas deferens and spleen) preincubated with (3)H-noradrenaline. Experiments using the OP(1) receptor-selective agonists DPDPE and DSLET, the OP(2)-selective agonists U50488H and U69593, the OP(3)-selective agonist DAMGO, the ORL(1) receptor-selective agonist nociceptin, and a number of selective antagonists showed that the noradrenergic axons innervating the occipito-parietal cortex possess release-inhibiting OP(3) and ORL(1) receptors, those innervating atria OP(1), ORL(1) and possibly OP(3) receptors, and those innervating the vas deferens all four opioid receptor types. Experiments using the non-selective CB agonists WIN 55,212-2 and CP 55,940 and the CB(1)-selective antagonist SR 141716A indicated that the noradrenergic axons of the vas deferens possess release-inhibiting CB(1) receptors. Presynaptic CB receptors were not found in the occipito-parietal cortex, in atria or in the spleen. Experiments using the non-selective beta-adrenoceptor agonist isoprenaline and the beta(2)-selective agonist salbutamol, as well as subtype-selective antagonists, demonstrated the occurrence of release-enhancing beta(2)-adrenoceptors at the sympathetic axons of atria and the spleen, but demonstrated their absence in the occipito-parietal cortex and the vas deferens. Experiments with bradykinin and the B(2)-selective antagonist Hoe 140 showed the operation of release-enhancing B(2) receptors at the sympathetic axons of atria, the vas deferens and the spleen, but showed their absence in the occipito-parietal cortex. The experiments document a number of new presynaptic receptor locations. They confirm and extend the existence of marked tissue and species differences in presynaptic receptors at noradrenergic neurons.     

γ-Hydroxybutters?ure — Neurotransmitter, Medikament und Droge

-Hydroxybuttersäure (GHB) ist eine natürlich vorkommende kurzkettige Fettsäure mit Neurotransmittereigenschaften. GHB war Anfang der 1960er Jahre als liquorgängiger GABA-Agonist synthetisiert worden und wird seitdem in der Anästhesie und Intensivmedizin zur Narkoseeinleitung und Sedierung verwendet. Später zeigte sich, dass GHB auch physiologisch vorkommt und spezifische GHB-Rezeptoren im ZNS existieren. Seit kurzem wird GHB auch beim Alkoholentzug und in der Behandlung von Schlafstörungen eingesetzt. Aufgrund von mild euphorisierenden und sedierenden Eigenschaften hat sich der Konsum von GHB — vertrieben unter Bezeichnungen wie Liquid Ecstasy — in der jugendlichen Musikszene in den letzten Jahren rasch ausgebreitet. Insofern ist es wichtig die Symptome einer GHB-Intoxikation zu kennen, da eine Vergiftung bei GHB-Konsumenten häufig auftritt und GHB schwierig nachzuweisen ist. Fallberichte aus den letzten Jahren belegen zudem die Gefahr, eine Abhängigkeit zu entwickeln, sowie die Gefahr eines potenziell letalen Entzugssyndroms.     

Autoantibodies against complement receptor 1 (CD35) in SLE, liver cirrhosis and HIV-infected patients

The acquired loss of CR1 (CD35) on erythrocytes in specific autoimmune diseases and chronic infections may be due to autoAb against CR1. An ELISA using rCR1 was established to measure antiCR1 IgG autoAb. Plasma containing alloAb to polymorphism on CR1 (Knops blood group Ab) reacted strongly against rCR1 and were used as positive controls. AntiCR1 Ab was found in 3/90 (3.5%) plasma samples from healthy blood donors. The binding of these Ab was not inhibited by high salt concentrations. AntiCR1 Ab were present in the IgG fractions of plasma, and they bound to rCR1 on Western Blot. Affinity chromatography on rCR1-sepharose depleted the plasma of antiCR1, and the acid-eluted fractions contained the antiCR1 Ab. An increased frequency of antiCR1 autoAb was found in patients with SLE (36/78; 46%), liver cirrhosis (15/41; 36%), HIV infection (23/76; 30%) (all P < 0.0001), and in patients with anticardiolipin Ab (4/21; 19%, P < 0.01) multiple sclerosis (7/50; 14%, P < 0.02), and myeloma (autoAb (8/56; 14%, P < 0.02), but not in those with acute poststreptococcal glomerulonephritis (1:32; 3%). Because C1q binds to CR1, antiC1q Ab were analysed in the same patients. There was no correlation between levels of antiC1q and antiCR1 autoAb. In HIV patients, levels of antiCR1 did not correlate with low CR1 levels expressed on erythrocytes or soluble CR1 in plasma. The binding of antiCR1 autoAb to rCR1 fixed on ELISA plates was not inhibited by soluble rCR1 or by human erythrocyte CR1, in contrast to alloAb and one SLE serum, which induced partial blockade. Thus, antiCR1 autoAb recognize mostly CR1 epitope(s) not present on the native molecule, suggesting that they are not directly involved in the loss of CR1. Rather antiCR1 autoAb might indicate a specific immune response to denatured CR1.     

The sensitivity of adrenergic varicosities to the 3H-noradrenaline-releasing effect of potassium

Summary After the loading of incubated, homogeneously innervated tissues with ³H-noradrenaline (monoamine oxidase and catechol-O-methyl transferase inhibited, calcium-containing solution) high K⁺ released the ³H-amine from adrenergic varicosities. In paired experiments the sensitivity of rat atria to high K⁺ exceeded that of vasa deferentia.In the rat vas deferens the releasing effect of high K⁺ was enhanced by drugs or procedures which induce a carrier-mediated outward transport of ³H-noradrenaline, i.e., by ouabain, by glucose deprivation and by hypoxia. — In the presence of extracellular calcium desipramine failed to affect the releasing effect of high K⁺ (except in the absence of glucose or during hypox1a), but in the absence of calcium desipramine reduced it. Apparently, whenever the axoplasmic levels of ³H-noradrenaline are increased, high K⁺ is able to induce some carrier-mediated outward transport of the 3H-amine.It is suggested that organ differences with respect to the sensitivity to high K⁺ may well be due to hypoxia (plus some lack of glucose) of those varicosities that had been loaded with ³H-noradrenaline. The risk of storage of ³H-noradrenaline in hypoxic varicosities appears to be greater in incubated than in perfused organs, and in the former it is greater in sparsely than in densely innervated tissues.Abbreviations COMT catechol-O-methyl transferase - FRL fractional rate of loss - MAO monoamine oxidase Supported by the Dr. Robert Pfleger-Stiftung and the Deutsche Forschungsgemeinschaft (SFB 176) Send offprint requests to U. Trendelenburg at the above address     

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Distinct mixtures of muscarinic receptor subtypes mediate inhibition of noradrenaline release in different mouse peripheral tissues, as studied with receptor knockout mice

The muscarinic heteroreceptors modulating noradrenaline release in atria, urinary bladder and vas deferens were previously studied in mice in which the M(2) or the M(4) muscarinic receptor genes had been disrupted. These experiments showed that these tissues possessed both M(2) and non-M(2) heteroreceptors. The analysis was now extended to mice in which either the M(3), both the M(2) and the M(3), or both the M(2) and the M(4) genes had been disrupted (M(3)-knockout, M(2/3)-knockout and M(2/4)-knockout). Tissues were preincubated with (3)H-noradrenaline and then stimulated electrically (20 pulses per 50 Hz). In wild-type atria, carbachol (0.01-100 microM) decreased the electrically evoked tritium overflow by maximally 60-78%. The maximum inhibition of carbachol was reduced to 57% in M(3)-knockout and to 23% in M(2/4)-knockout atria. Strikingly, the effect of carbachol was abolished in M(2/3)-knockout atria.In wild-type bladder, carbachol (0.01-100 microM) reduced the evoked tritium overflow by maximally 57-71%. This effect remained unchanged in the M(3)-knockout, but was abolished in the M(2/4)-knockout bladder. In wild-type vas deferens, carbachol (0.01-100 microM) reduced the evoked tritium overflow by maximally 34-48%. The maximum inhibition of carbachol was reduced to 40% in the M(3)-knockout and to 18% in the M(2/4)-knockout vas deferens. We conclude that the postganglionic sympathetic axons of mouse atria possess M(2) and M(3), those of the urinary bladder M(2) and M(4), and those of the vas deferens M(2), M(3) and M(4) release-inhibiting muscarinic receptors.     

Mechanism of action of indirectly acting sympathomimetic amines

The mode of action of indirectly acting sympathomimetic amines was analysed in the rat vas deferens (preloaded with 3H-(-)-noradrenaline). When monoamine oxidase (MAO), catechol-O-methyltransferase and vesicular uptake were inhibited (i.e., when the concentration of 3H-noradrenaline in the axoplasm was high), all substrates of neuronal uptake induced a carrier-mediated outward transport of 3H-noradrenaline, in strict dependence on the Km for neuronal uptake of the substrate. However, when MAO and vesicular uptake were not inhibited, some of the substrates of neuronal uptake were better releasers of 3H-noradrenaline than others; obviously, when the axoplasmic 3H-noradrenaline concentration is very low (intact vesicular uptake, intact MAO), a 'mobilization' of vesicular 3H-noradrenaline is a prerequisite for substantial release.