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M Formaniak

Publications and source records attributed to M Formaniak.

6 recordsLinked to original sources
PubMed1984

Calcium channel activity in rat brain synaptosomes: effects of neuroleptics and other factors regulating phosphorylation and transmitter release.

Neuroleptic drugs inhibit depolarization-induced Ca uptake in nerve endings, having IC50 values in the micromolar range. Dopamine and a variety of other substances including opiates and PGE1 are inactive. The effect is probably not mediated by the interaction of the neuroleptics with calmodulin, which itself is a potent inhibitor of stimulated Ca uptake. Dibutyryl cyclic AMP, but not fluoride, increases K+-stimulated Ca uptake. Phosphatidic acid, which is an intermediate in transmitter-stimulated phosphatidylinositol turnover, acts as a Ca ionophore in nerve endings and enhances K+-stimulated Ca uptake at a relatively low concentration. Carbamyl choline, a known stimulator of phosphatidylinositol turnover, did not, however, cause a significant increase in K+-stimulated Ca uptake. Treatment of the nerve ending fraction with relatively small amounts of phospholipase A2 greatly inhibited depolarization-induced Ca uptake, demonstrating the importance of phospholipids for the functioning of the potential-dependent Ca channel in nerve endings. These studies suggest that the regulation of voltage-sensitive Ca channels in nerve endings may be one mechanism controlling transmitter release.

Animals↗
PubMed1984

Effect of 2450 MHz microwave energy on the blood-brain barrier to hydrophilic molecules. A. Effect on the permeability to sodium fluorescein.

Significantly elevated levels of sodium fluorescein (MW 376) were found only in the brains of conscious rats made considerably hyperthermic (colonic temperatures greater than 41.0 degrees C) by exposure to ambient heat (42 +/- 2 degrees C) for 90 min or 2450 MHz CW microwave energy at 65 mW/cm2 (SAR approximately equal to 13.0 W/kg) for 30 or 90 min. For microwave-exposed rats, fluorescein levels within the cortex and hypothalamus appeared to increase with increasing duration of exposure. This trend was not apparent in the cerebellum or medulla. Exposure to ambient heat resulted in increased fluorescein with the cortex, hypothalamus and medulla, but not the cerebellum, and, in general, ambient heat was not as effective as microwave energy in raising tracer concentrations within the brain. By far the greatest elevation of fluorescein dye in the brain occurred in those animals whose blood-brain barrier had been opened osmotically by intracarotid injection of 10 M urea. It is suggested that increased levels of sodium fluorescein found in the brain tissue of ambient heat and microwave-exposed rats most likely represent technically derived artifact and not a breakdown of the blood-brain barrier.

Animals↗
PubMed1984

Depolarization-induced increase in synaptosomal membrane calcium monitored by chlorotetracycline fluorescence.

Chlorotetracycline (CT) was used as a fluorescent probe for membrane calcium with intact synaptosomes. The net increase in fluorescence intensity at 520 nm, which is a measure of membrane-bound Ca, increases with increasing Ca, saturating in the millimolar range. Membrane Ca can also be detected in the absence of added external Ca. Potassium-induced depolarization of synaptosomes leads to an increase in membrane Ca, reaching a new steady-state value within 5 min. Neither opiates nor phenytoin affected synaptosomal membrane Ca. Relatively high concentrations of chlorotetracycline increased depolarization-induced uptake of 45Ca into synaptosomes. The data suggest that the Ca-CT complex binds to synaptic plasma membranes, and that depolarization-induced Ca influx results in increased Ca binding to the internal surface of the plasma membrane and/or other internal membranes.

Animals↗
PubMed1983

Effects of opiates on synaptosomal calmodulin and calcium uptake.

Acute opiate administration in vivo increases the level of cytoplasmic calmodulin in isolated rat brain synaptosomes. These synaptosomes do not, however, display decreased K+-stimulated 45Ca uptake in vitro. Opiates affect neither cytoplasmic calmodulin nor Ca uptake after incubation of synaptosomes with the drugs in vitro. In contrast to the interpretation of electrophysiological data, these results suggest that the observed inhibition by opiates of the release of several transmitters may not be mediated by presynaptic opiate receptors that inhibit Ca uptake.

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