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Biomedical subjects

R Schulz

Publications and source records attributed to R Schulz.

At least 577 records · Page 32Linked to original sources
PubMed1980

Interaction of amphetamine and naloxone in feeding behavior in guinea pigs.

Chronic naloxone treatment of schedule-fed guinea pigs caused an initial anorexia followed by a resumption of food and water intake, despite the continued presence of the narcotic antagonist. During this state of chronic naloxone treatment, amphetamine exerted a similar degree of anorexia to that in animals not pretreated with naloxone. In contrast, amphetamine tolerant guinea pigs exhibited supersensitivity to naloxone with respect to feeding behavior. Since chronic amphetamine exposure results in an increased level of beta-endorphin in the hypothalamus it is suggested that an enhanced endorphinergic activity compensates for the effect of amphetamine on feeding mechanisms.

Amphetamine↗
PubMed1980

Inquiry into endorphinergic feedback mechanisms during the development of opiate tolerance/dependence.

Met-enkephalin and beta-endorphin levels were determined in the pituitary and brain of rats after treatment for several weeks with either agonists of high receptor affinity, such as levorphanol and etorphine, or with the narcotic antagnoist naloxone. Long-term activation of opiate receptors failed to change the endorphin levels in restricted areas of brain and pituitary, although a high degree of tolerance/dependence is apparent in those animals. Chronic blockade of opiate receptors by naloxone also fails to affect endorphin levels in the pituitary, but selectively increases metenkephalin levels in the striatum. The present data do not support the notion of negative feedback mechanisms to regulate endorphingergic functions during the development of opiate tolerance/dependence.

Animals↗
PubMed1980

Acute and chronic ethanol treatment changes endorphin levels in brain and pituitary.

Acute ethanol administration increased methionine-enkephalin (met-enkephalin) and beta-endorphin levels in distinct areas of the rat brain, whereas chronically supplied ethanol caused a depression of met-enkephalin and beta-endorphin levels in most of the brain areas investigated. The beta-endorphin content of the intermediate/posterior lobe of the pituitary of rats and guinea pigs decreased by 70%. Withdrawal of ethanol resulted in a complete recovery of endorphin levels in brain and pituitary within two weeks. Whether the observed alterations in endorphin concentrations are causally related to the primary mechanisms underlying alcohol dependence is uncertain, since no obvious signs of physical dependence were observed in treated animals.

Alcoholism↗
PubMed1980

Differential effects of potassium on the potency of different opioids in the mouse vas deferens.

The effect of potassium on the potency of different opioids to inhibit electrically evoked twitches of the mouse vas deferens has been studied. In general, opioids lose activity as the concentration of potassium increases. Distinct differences, however, were observed between specific opiate receptor agonists. Least sensitive to the effect of potassium proved mu- and delta-opiate receptor agonists, showing only a 2-fold increase in the concentration required to cause a half-maximal inhibition at 14 mM K+. In contrast, the supposed dynorphin receptor/kappa-receptor agonists exhibited at this concentration up to an 8-fold loss of potency. Dynorphin1-13 was found to be intermediate with a 5-fold loss of inhibitory activity. These data suggest a modulatory action of potassium for dynorphin- and kappa-receptors.

Animals↗
PubMed1980

Inhibition of neuroeffector transmission by morphine in the vas deferens of naive and morphine-treated mice.

1 The amplitude of excitatory junction potentials (e.j.ps) recorded intracellularly from smooth muscle cells of the mouse vas deferens varied with the strength of stimulation. Normorphine (0.4, 2 and 10 microM) shifted the stimulus-response curve to the right, without any change in slope. This shift of the curve was proportional to the concentration of the opiate in the bath. Naloxone (0.4 and 2 microM) antagonized this effect of normorphine. 2 The action of normorphine (2 and 10 microM) was studied in vasa deferentia prepared from control mice and mice that had been implanted with morphine pellets. Both groups of tissues were continuously exposed to a low concentration of normorphine (0.4 microM), to simulate the plasma concentration in the morphine-treated mice. Addition of 10 microM normorphine produced a parallel displacement of the curve in vasa deferentia from control animals, and a non-parallel displacement in tissues from morphine pellet-implanted mice. In the preparations from morphine-treated mice a pronounced degree of tolerance to normorphine was observed at a low stimulus strength. 3 Naloxone (0.4 and 2 microM) had a greater effect on vasa deferentia prepared from morphine-treated animals than on tissues from control mice, when both organs were continuously exposed to 0.4 microM normorphine. The difference in the effect of the antagonist in the two groups of preparations was absent when the incubating solution contained 2 microM normorphine. 4 It is concluded that a low intensity of stimulation the e.j.ps are more readily depressed by normorphine and also the degree of tolerance displayed is larger than at a high intensity of stimulation.

Animals↗
PubMed1980

Some aspects of opiate receptors.

There is accumulating evidence that the existence of various endorphins is parallelled by the existence of multiple opiate receptors for these different ligands. At present, it appears that opiate binding sites in the mouse vas deferens are specifically sensitive to enkephalins, while the receptors of the vas deferens of the rat are selectively sensitive to beta-endorphin. Although enkephalin is present in the guinea pig ileum, it is not yet known if there are other endogenous ligands that preferentially combine with the mu-receptors located in this tissue. We suggest that a preference of the particular opiate receptors for specific ligands with different properties (e.g., their different susceptibility to enzymatic degradation) could characterize these binding sites as receptors for either neurotransmitters or hormones.

Animals↗
PubMed1980

[Diagnosis and therapy of malignant parenchymal kidney tumors].

We think that the present paper insistently demonstrates the fact which is acknowledged by all but followed only by few how important is a unitary classification of the renal tumours in order to perform scientifically proved comparisons and valuations in all branches of the treatment of renal tumours including the results of the therapy. On the basis of the classification of our patients according to the TNM-system we could prove that the best results in the operative removal of the kidney with following irradiation were achieved in the categories T1 and T2, particularly when there were not yet present any metastases distant from the primary tumour.

Adenocarcinoma↗
PubMed1979

Sporulation of mitochondrial respiratory deficient mit- mutants of Saccharomyces cerevisiae.

The role of mitochondrial protein synthesis, electron transport, and four specific mitochondrial gene products on sporulation were studied in respiratory deficient mit- mutants. These mutants were isolated in an op 1 strain and localized on the mitochondrial genome by petite deletion mapping. All 153 mutations studied could be assigned to the four mitochondrial regions OXI1, OXI2, OXI3 and COB, known to affect cytochrome c oxidase and cytochrome b. The specific loss of one mitochondrially translated polypeptide was found in some mutants of each locus: OXI1--cytochrome c oxidase subunit 2, OXI2--subunit 3, OXI3--subunit 1, and COB--cytochrome b. The ability of diploid mit- mutants to sporulate was systematically investigated. About one third of the mutants, representing three loci, were incapable of forming spores. All other cultures produced either respiratory competent mit+ tetrads, both mit+ and mit- tetrads, or only mit- tetrads. Mutants forming mit- tetrads mapped in all four loci. These results demonstrate that in contrast to petite mutants some mit- mutants have retained the ability to perform meiosis and sporulation.

DNA, Mitochondrial↗
PubMed1979

Centrally and peripherally mediated inhibition of intestinal motility by opioids.

Intracerebroventricularly injected morphine is 50-fold more potent in arresting intestinal peristalsis in rats, mice or guinea pigs than morphine administered systemically. Using quaternary naloxone as narcotic antagonist, it has been demonstrated that the peripheral pathway of the centrally mediated constipatory effect of morphine does not involve opioid peptidergic mechanisms. Further, this effect is not due to the release of opioid peptides from the pituitary, since hypophysectomy fails to affect the antipropulsive activity of morphine. On the other hand, the intestinal motility can be affected directly by activation of opiate receptors located in the gut. This was best demonstrated with loperamide, which exhibits predominantly a peripheral site of action. Thus, two mechanisms of the action of morphine on gastrointestinal propulsive activity have been demonstrated. One arises in the central nervous system (CNS) and is mediated peripherally not by opioid peptidergic pathways, whereas the other is due to a direct action of morphine on the gut.

Animals↗