High-affinity binding ofβ-alanine to cerebral synaptosomes might involve glycine-receptors

Summary High-affinity, Na⁺-independent binding of -alanine to a synaptosomal fraction of rat brain was potently inhibited by glycine and by some other -amino acids, but not by taurine or GABA. This binding mechanism, which was also sensitive to both bicuculline and strychnine, might involve synaptic receptors for both -alanine and glycine.This study was supported in part by Centro Ramón y Cajal and Fundacion Juan March.     

Control of obesity inA vy /a mice by 5α-androstan-17-one

Summary Treating VY/WfL-A ^vy /a mice with 5-androstan-17-one, a mammalian glucose-6-phosphate dehydrogenase inhibitor, prevented the mice from becoming obese. The weight difference between treated and controlA ^vy /a mice was mainly due to a decreased accumulation of triacylglycerol. The compound did not suppress appetite, had no detectable toxicity and did not affect the lipogenesis rates in the liver and carcass. The weight-controlling effect of 5-androstan-17-one inA ^vy /a mice was reversible upon withdrawal of treatment.The authors wish to thank Mr W.R. Gibson and Drs C.G. Culbertson and P.N. Harris for performing the pathological examinations.     

Influence of the thymus on the incidence of secondary and parabiotic disease

Summary The secondary disease in PF₁ strain combination depends upon the immune status of both partners. It is most clearly expressed if both donors and recipients are immunologically crippled by thymectomy and irradiation. Conspicuous reduction in the immune potential of parental parabionts induced by thymectomy and irradiation displayed their marked incidence of parabiotic death.     

Genetic basis of susceptibility for development of neoplasms following treatment with N-methyl-N-nitrosourea (MNU) or X-rays in the platyfish/swordtail system

Summary Specific genotypes of the xiphophorine fish develop neoplasms following treatment with N-methyl-N-nitrosourea or X-rays. Several of these neoplasms can be related to the presence of specific chromosomes. The implications of these findings are discussed.Supported by Deutsche Forschungsgemeinschaft through Sonderforschungsbereich 103 Zellenergetik und Zelldifferenzierung, Marburg (projects C 9 and C 10), and by Justus-Liebig-Universität Giessen. We are indebted to Prof. K. Frese, Veterinär-Pathologisches Institut, Giessen and Dr H. D. Mennel, Pathologisches Institut, Freiburg, for their help in the classification of neoplasms. We furthermore thank K. Klinke for breeding the fish. Dedicated to Prof. C. Kosswig on the occasion of his 75^th birthday.The paper contains parts of the dissertations of S. Abdo, J. Haas and G. Kollinger.supported by the Egypt ministry of education.     

Action ofβ-(4-chlorophenyl-GABA) on uptake and metabolism of GABA in different subcellular fractions of rat brain

Summary -(4-chlorophenyl)-GABA, a GABA mimetic compound, acts as an inhibitor of GABA metabolism in both synaptosomal and extrasynaptosomal compartments. It has no significant action on GABA or Glu uptake by synaptosomes.     

Inhibition of noradrenaline release from sympathetic nerves by pentobarbital

Summary Pentobarbital concentrations of 10–100 M selectively inhibited the noradrenaline release evoked by activation of the nicotinic receptors on the terminals sympathetic nerves of the rabbit heart. Higher concentrations also decreased the noradrenaline release induced by KCl or by electrical stimulation of the nerve axons.This paper is dedicated to Professor Dr. G. Malorny on the occasion of his 65th birthday.Acknowledgment: We thank Mrs G. Thielecke for technical assistance.     

Effect of dibutyryl cyclic AMP and analogs on the rate of contractions of myocytes in culture

Summary ²O,⁶N-butyryl, 3, 5-cyclic monophosphate (dibu cAMP) when added to fetal rat heart cells in culture inhibits myocyte contraction. This inhibition is 100, 84 and 51% complete when the dibu cAMP concentration used is 2, 0.2 and 0.02 mM, respectively. The potency of dibu cAMP derivatives in myocyte contraction inhibition follows the order, dibu cAMP> ⁶N-bu cAMP> ²O-bu cAMP=AMP>butyrate. The inhibition caused by the first three chemicals is greater than 70%.The author was a Moss Heart Fellow and acknowledges the technical assistance of Ms Martha Peet. This work was supported in part by the American Heart Association, National Science Foundation and American Cancer Society.     

Polyoxin fungicides: Demonstration of insecticidal activity due to inhibition of chitin synthesis

Summary Polyoxin A, a selective inhibitor of chitin synthetase, was found to be insecticidal when injected into the abdomen of grasshoppers nymphs, with an LD₅₀ of 1.26±0.20 g per insect. Symptomatology and the absence of any toxicity toward adult insects indicate that toxicity is due to interference with cuticle deposition.Acknowledgment. I thank Henry Bork for his expert technical assistance.     

Action of glutamic acid and of some glutamate analogues on the molluscan central neurones

Summary The effects of L-glutamic acid and of some glutamate analogues have been studied on the central nervous system of the snailHeobania vermiculata, using conventional electrophysiological techniques. The glutamate H-response had the mean equilibrium value of-(57±4) mV and was associated with a Cl^– conductance change. The D-response to glutamate application showed an involvement of sodium ions. Aspartate was agonist of glutamate action and displayed similar equilibrium value of the H-response, whereas quisqualate H-response was non-invertible.The authors wish to express their thanks to Prof. A. Curatolo for his continual interest and advice, and to Dr J. Stinnakre for the criticism of the text.     

The timing of cyclophosphamide therapy in tumor-bearing rats affects the resistance to tumor challenge in survivors

Summary Cyclophosphamide given to rats 2 or 5 days after an injection of Yoshida ascites sarcoma cured approximately the same proportion of animals, but the resistance to a subsequent tumor challenge was found only in rats treated with the drug 5 days after tumor injection.