Search Results - (Author, Cooperation:E. M. Meyer)

2011-12-14

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

Animals ; Auditory Cortex/cytology/drug effects/*physiology ; Conditioning, Classical/drug effects/*physiology ; Electroshock ; Extremities/innervation/physiology ; Fear/drug effects/*physiology/*psychology ; Interneurons/cytology/drug effects/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Models, Neurological ; Nerve Net/cytology/drug effects/physiology ; Neural Inhibition/drug effects/physiology ; Neural Pathways/cytology/drug effects/*physiology ; Nicotinic Antagonists/pharmacology ; Pyramidal Cells/drug effects/physiology ; Receptors, Nicotinic/metabolism

2018-02-27

Wiley-Blackwell

0007-1048

1365-2141

Medicine

1471-4159

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Abstract: The effects of acetylethylcholine mustard and its aziridinium derivative (AMMA) on acetylcholine (ACh) release and [3H]quinuclidinyl benzilate (QNB) binding were studied in rat cortical synaptosomes. After incubation for 5 min at 37°C, AMMA reduced [3H]QNB binding with an IC50 of 9 μM. Following incubation for 5 min with 50 μM AMMA and washing, there was a 62% reduction in the [3H]QNB binding capacity with no change in the KD value for the remaining receptors, a result indicating the irrevers-ibility of the AMMA binding. AMMA and oxotremorine both reduced the basal and 30 mM K+-induced release of newly synthesized [3H]ACh in dose-dependent manners over a 2.5-min period. At identical 50 μM concentrations, AMMA produced a much longer inhibition of basal [3H]ACh release than oxotremorine did. The inhibition of basal and 30 mM K+-induced [3H]ACh release by AMMA (10–250 μM) was blocked by 2 μM atropine during a 2.5-min release incubation, but not during a 30-min release in cubation. After synaptosomes were treated with 50 μM AMMA for 5 min and the unbound drug was washed out from the tissue, [3H]ACh release (basal and K+-induced) was reduced. AMMA (50 μM) reduced high-affinity choline uptake and ACh synthesis by 〉90% in this tissue, but these effects did not account for the [3H]ACh release inhibition, because (a) they were not atropine sensitive and (b) hemi-cholinium-3 had no effect on [3H]ACh release under the conditions used in these studies, i.e., after extracellular [3H]choline was washed out. Taken together, these results suggest that AMMA may be an irreversible agonist at pre-synaptic muscarinic autoreceptors.

Electronic Resource

1471-4159

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Abstract The capacity of calcium ions to trigger acetylcholine release was studied in cerebral cortical synaptosomes from adult (6-month-old) and senescent (24-month-old) rats, using a calcium ionophore, A23187, that bypasses voltage-sensitive calcium channels. The potency but not the efficacy of the A23187 was reduced with respect to releasing acetylcholine (ACh) in the aged animals. There was no age-related difference in the synthesis of ACh or potency of the ionophore with respect to increasing 45calcium uptake. These results suggest that aging reduces the sensitivity of cerebral cortical nerve terminals to calcium-triggered ACh-release.

Electronic Resource

1471-4159

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Abstract: [3H]Acetylcholine efflux and Na+-K+ ATPase ion pump activity were measured concomitantly in rat cortical synaptosomes. Ouabain (500 μM), strophanthidin (500 μM). and parachloromercuribenzene sulfonate (500 μM) each inhibited ouabain-sensitive 86Rb uptake and elevated [3H]acetylcholine release independently of the external calcium concentration. Veratridine (10 μM), electrical field stimulation (60 V, 60 Hz, 5-ms pulse duration), or the calcium ionophore A23187 (10μg/ml) also inhibited ouabain-sensitive 86Rb uptake and released [3H]acetylcholine, but via a calcium-dependent process. Veratridine-induced [3H]acetylcholine release and ion pump inhibition were correlated over a wide range of drug concentrations and both effects were blocked by pre-treatment with tetrodotoxin (1 μM). The rate of [3H]acetyl-choline efflux from superfused synaptosomes was increased within 15 s of exposure to ouabain, strophanthidin, veratridine, A23187, or field stimulation, while ouabain-sensitive 86Rb uptake was significantly decreased within a similar interval. These results suggest that [3H]acetylcholine release is due at least in part to inhibition of Na+-K+ ATPase.

Electronic Resource

1749-6632

Blackwell Publishing Journal Backfiles 1879-2005

Natural Sciences in General

Electronic Resource

0257-8972

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics

Physics

Electronic Resource

1432-1440

Lymph node morphology ; Tumor immunology ; Prognostic parameters ; Lymphknotenmorphologie ; Tumorimmunologie ; Prognostische Parameter

Springer Online Journal Archives 1860-2000

Medicine

Zusammenfassung Der Versuch einer Ordnung der histologischen, histomorphometrischen und histochemischen Beobachtungen über die Reaktionen in den regionären Lymphknoten bei bösartigen Tumoren, wie sie bei Tierexperimenten und beim Menschen mitgeteilt worden sind, führt unter Einbezug neuer Befunde an autochthonen experimentellen Rattenkarzinomen des Magen-Darm-Kanals zu folgenden möglichen Parametern: 1) Die Entwicklung von Keimzentren und die Plasmazellreaktion als morphologische Korrelate für lokal ablaufende humorale Immunantworten können tumorspezifische Lymphknotenreaktionen darstellen. Im Tierexperiment erreichen sie ihr Maximum in Spätstadien des Tumorwachstums; bei Tumoren des Menschen ist ihre Inzidenz und auch ihre prognostische Bedeutung unterschiedlich, je nach Tumorstadium und Tumorart. 2) Die Sinushistiozytose ist eine Lymphknotenreaktion ohne spezifische immunologische Bedeutung und ohne gesicherte prognostische Relevanz. 3) Sarkoid-ähnliche histiozytäre Granulome sind wahrscheinlich Zeichen einer tumorspezifischen Immunreaktion, bei der Makrophagen durch T-Lymphozyten aktiviert wurden; sie sind ein günstiges prognostisches Zeichen. 4) Die Hyperplasie des Parakortex infolge einer vermehrten Akkumulation von Lymphozyten und gegebenenfalls von Immunoblasten ist das morphologische Substrat T-zellvermittelter Immunreaktionen. Diese Lymphknotenreaktion findet sich typischerweise während der Frühstadien experimenteller Tiertumoren; bei Tumoren des Menschen hat sie generell eine günstige prognostische Bedeutung. 5) Die Involution der T-Zell-Areale infolge einer Verarmung an Lymphozyten und die auf einer Histiozyten-Vermehrung bei gleichzeitiger Lymphozyten-Verarmung beruhende Entwicklung von Parakortikalknoten sind besonders charakteristisch für Lymphknoten aus dem Bereich fortgeschrittener Tumoren. Beide Reaktionsmuster lassen sich in Zusammenhang mit einer Funktionseinschränkung des T-Zell-Systems verstehen. Diese Bestandsaufnahme des Reaktionsspektrums der verschiedenen Lymphknotenkompartimente deutet auf ein mögliches histologisches Immunstaging bei bösartigen Tumoren, das als zusätzliche Entscheidungshilfe für die Therapieplanung dienen könnte.

Summary Histological, histomorphometrical and histochemical data on the response of regional lymph nodes to tumor development, as recorded in experimental and clinical studies, were coordinated and supplemented by recent findings in experimentally induced autochthonous carcinomas in the rat gastrointestinal tract. The attempted correlation led to the definition of several prognostic parameters: 1) The development of germinal centers and the plasmocytic reaction in tumor draining nodes are morphological expressions of active humoral immune responses that may be specifically directed against the tumor. These reactions attain their maximum usually during late stages of tumor development. Their incidence and prognostic significance may vary depending upon the stage and the type of tumor. 2) Sinus histiocytosis is an immunologically nonspecific lymph node response with debatable prognostic significance. 3) Granulomatous sarcoid-like lesions may be understood as signs of an immunologically mediated antitumor response of macrophages activated by T lymphocytes. They are indicative of a favorable prognosis. 4) Paracortical hyperplasia, characterized by an increased population of lymphocytes and eventually immunoblasts, is an expression of an active T-cell reaction. This reaction occurs typically during early stages of experimental tumors. Correspondingly, it is of favorable prognostic significance in human tumors. 5) Lymphocytic depletion and nodular alteration of T-cell areas, with increased histiocytic infiltration, are reactions most often seen in the draining nodes of an advanced tumor. Both seem to coincide with depression of the cell-mediated immune reactivity. The present assessment of the reactive behavior of diverse lymph node compartments may serve as a first pointer to the proposed histologic immunostaging of malignant tumors.

Electronic Resource

1432-1335

Laboratory mouse ; Malignant lymphomas ; Classification ; Immunocytology ; Cytochemistry

Springer Online Journal Archives 1860-2000

Medicine

Summary We review techniques used to classify malignant lymphomas of the laboratory mouse. Besides an initial morphologic classification according to the Rappaport scheme for human lymphomas, individual tumor types were further subclassified by use of immunocytological T- and B-cell determinations as well as by histochemical procedures. The results, which allow a certain appraisal of the maturation stage of lymphoma cells, are discussed taking as examples six different experimental mouse lymphomas.

Electronic Resource

1573-6903

Springer Online Journal Archives 1860-2000

Medicine

Abstract Synaptosomal acetylcholine synthesis was found to be dependent on the presence of Na+-dependent HC-3 sensitive choline transport at low (5.5 mM) and high (35 mM) K+ concentrations. However, at 5, 20, and 100 μM choline, choline phosphorylation was proportional to total choline uptake, in the presence or absence of high affinity transport. Only in the presence of eserine (50 μM) did acetylcholine synthesis increase as the choline concentration was elevated from 20 μM to 100 μM, and this effect was observed at low and high K+ concentrations. Our results suggest that: 1) the synthesis of non-surplus synaptosomal ACh is dependent on high affinity choline transport; and 2) choline is equally likely to be phosphorylated after being taken up by low or high affinity transport.

Electronic Resource

1573-6903

Acetylcholine ; choline ; liposomes ; phospholipids

Springer Online Journal Archives 1860-2000

Medicine

Abstract We investigated the effects of various phospholipids on the presynaptic levels of newly synthesized [3H]acetylcholine (ACh) in rat cerebral cortical synaptosomes. When administered as small unilamellar vesicles (200–500 Å diameters) dipalmitoylphosphatidylcholine (DPPC) reduced [3H]ACh levels in concentration and time-related manners, while increasing the efflux of labelled choline to a similar extent. The reductions in synaptosomal [3H]-ACh levels induced by DPPC (3 mg/ml) were found in the cytosolic S3 but not microsomal P3 fraction, arguing for a cytoplasmic, nonvesicular site of action. DPPC-induced reductions in [3H]ACh levels were blocked by 100 μM eserine, a tertiary amine cholinesterase inhibitor, but not with 100 μM neostigmine, a quaternary ammonium inhibitor. Large unilamellar vesicles (2000–5000 Å diameters) consisting of soybean-phosphatidylcholine reduced [3H]ACh levels to the same extent that small vesicles did at the same concentration (3 mg/ml). Taken together, these results suggest that DPPC can fuse with membranes to increase the hydrolysis of cytoplasmic ACh via a small intra-terminal subpopulation of cholinesterases.

Electronic Resource

1573-6903

Springer Online Journal Archives 1860-2000

Medicine

Abstract We have investigated whether muscarinic receptors modulate the release of [3H]ACh elicited by secretagogues that act by different mechanisms in rat cerebral cortical synaptosomes. Oxotremorine (10 μM) reduced the calcium-dependent [3H]ACh release induced by mild K+-depolarization (10 and 15 mM K+), but not that by higher K+ concentrations. The ACh-release induced by A23187 (0.2–5 μg/ml), liposomes laden with 113 mM CaCl2, or 4-aminopyridine (1–10 mM) was not modulated by oxotremorine. Ouabain (100 μM)-induced release of [3H]ACh was reduced by oxotremorine in normal but not calcium-free KR, indicating that extracellular calcium-uptake but not Na+, K+-ATPase activity may be necessary for release-modulation. With respect to possible second messenger systems, dibutyrylcyclic AMP (0.1–2 mM), dibutyrylcyclic GMP (0.1–2 mM), forskolin (100 μM), and phorbol ester (0.3–3 μg/ml) were without effect on release or release-modulation. These results are consistent with an involvement of K+-channels and voltage-sensitive calcium-channels in the muscarinic release-inhibition process. They argue against an involvement of Na+, K+-ATPase, adenylate cyclase, guanylate cyclase, and phosphatidylinositol turnover in the release-modulation process.

Electronic Resource