Helen Majewski

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Protein kinase C (PKC), activated by either diacylglycerol and/or arachidonic acid, through the activation of presynaptic receptors or nerve or nerve depolarization is involved is involved in the enhancement of transmitter release from many neural types. This facilities is most likely mediated by the phosphorylation of proteins involved in vesicle dynamics(More)
Readers' eye movements were monitored as they read sentences containing noun-noun compounds that varied in frequency (e.g., elevator mechanic, mountain lion). The left constituent of the compound was either plausible or implausible as a head noun at the point at which it appeared, whereas the compound as a whole was always plausible. When the head noun(More)
1. The M1 selective muscarinic agonist, McNeil A 343, enhanced the electrically evoked release of noradrenaline from postganglionic sympathetic nerves in mouse atria. This has been found previously to be due to activation of muscarinic receptors of the M1 subtype, probably located on sympathetic nerve terminals. The present study investigated the signal(More)
Acetylcholine outflow can be modulated through inhibitory presynaptic muscarinic autoreceptors. This study was to identify which subtype is involved in mouse cortex. Five muscarinic antagonists and their ability to elevate stimulation-induced (S-I) acetylcholine outflow were tested in the presence of neostigmine, which decreased S-I outflow. The potency of(More)
1. McNeil A 343 (10 microM-30 microM) enhanced the fractional stimulation-induced (S-I) outflow of radioactivity from mouse isolated atria which had been incubated with [3H]-noradrenaline. The enhancing effect of McNeil A 343 was not altered by hexamethonium (300 microM) suggesting that it was not due to an action at nicotinic receptors. It is also unlikely(More)
Activation of protein kinase C (PKC) results in enhanced action-potential evoked release of a variety of transmitters. However, previous studies have suggested that acetylcholine release is poorly modulated by PKC compared to other transmitter types. We investigated the effect of stimulation conditions on PKC modulation of electrical stimulation-induced(More)
1. 3H-Noradrenaline was infused intravenously into pentobarbitone anaesthetized rabbits to reach a steady-state plasma 3H-noradrenaline level, from which the noradrenaline plasma clearance was calculated. The plasma level of endogenous noradrenaline was determined simultaneously and the rate of noradrenaline release was then derived. 2. Pargyline,(More)
Slices of rat kidney cortex were incubated in [3H]noradrenaline, then placed in a flow cell and subjected to electrical field stimulation. At a stimulation frequency of 5 Hz, both the alpha 2-adrenoceptor antagonist idazoxan (0.1 microM) and the alpha 1-adrenoceptor antagonist prazosin (0.1 microM) significantly enhanced the stimulation-induced (S-I)(More)
The history of conventional implicatures is rocky, their current status uncertain. It seems wise to return to their source and start fresh, with an open-minded reading of the original definition (Grice, 1975) and an eye open for novel support. Suppose the textbook examples (therefore, even, but and synonyms) disappeared. Where would conventional(More)
1. Interactions between dopamine receptors and protein kinase C (PKC) have been proposed from biochemical studies. The aim of the present study was to investigate the hypothesis that there is an interaction between protein kinase C and inhibitory D2-dopamine receptors in the modulation of stimulation-induced (S-I) dopamine release from rat striatal slices(More)