Anke Tomaszewski

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The anticancer drug cis-diammindichloroplatin (CDDP, cisplatin) causes severe side effects like peripheral sensitive neuropathy. The toxicity of CDDP has been linked to changes in intracellular calcium homeostasis ([Ca2+]i). Voltage activated calcium channel currents (ICa(V)) are important for the regulation of [Ca2+]i; therefore, this study was designed to(More)
Stannous dichloride (SnCl(2)) occurs in the environment where it has been especially enriched in aquatic ecosystems. Furthermore, it is used in food manufacturing (e.g. for stabilizing soft drinks or as an anti-corrosive substance) and in nuclear medicine where it is employed as a reducing agent for technecium-99m (99mTc) and therefore is applied(More)
Taurine applied to rats intracerebroventricularly in doses 0.1--3.0 mg increased ACh level and decreased ACh synthesis in the cerebral cortex. In the striatum ACh level was increased after doses of 0.1--3.0 mg and ACh synthesis was decreased after 0.01--3.0 mg. In the hippocampus taurine appeared to decrease both ACh level (0.5--3.0 mg) and synthesis(More)
The investigations were carried out on white rats determining the level and synthesis of acetylcholine (ACh) in the cerebral cortex, striatum, and in some experiments also in the brain stem. Thyroxine administered subcutaneously increased ACh synthesis in the cerbral cortex and reduced it in the striatum without changing the level of ACh in these(More)
Intracerebroventricular injection of glycine elevated the level and synthesis rate of acetylcholine and the activity of choline acetyltransferase in the striatum. Administration of strychnine alone did not change these parameters, but pretreatment with strychnine abolished the stimulatory effect of glycine on the cholinergic system of the rat striatum.(More)
Glycine, 0.5 mg icvtr, elevated the striatal acetylcholine (ACh) level 30 and 45 min after the injection, and accelerated ACh synthesis 15-45 min after the administration. Only doses of 0.25 and 0.5 mg produced these effects. Glycine elevated the choline acetyltransferase activity in the striatum, but did not affect acetylcholine esterase. Studies in vitro(More)
Kainic acid applied intracerebroventricularly at a dose of 0.1 micrograms/rat decreased the ACh level inthe cortex and increased it in the striatum 3 h after the injection. ACh release 3 h from the moment of injection was depressed in both examined structure. 1, 5 and 20 days after injection, ACh level and release were depressed in the striatum.
Bicuculline (BK) administered into the lateral ventricle (i.v.c.) of Wistar rats in a dose of 10 microgram reduced the level and the intensity of acetylcholine (ACh) synthesis in rat brain cortex. On the other hand, Bk administered in the same way in doses of 1, 5 and 10 microgram decreased the activity of acetylcholine esterase. Gamma-aminobutyric acid(More)
The aim of the present work was to explain the mechanism of the stimulating effect of adrenaline (A) on acetylcholine (ACh) synthesis. This action is exerted most probably through the beta- adrenergic receptors, since propranolol and oxprenolol inhibit the stimulating effect of adrenaline on acetylcholine synthesis in the rat cerebral cortex in vitro.(More)
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