The effects of ethanol and chlorpromazine on the passive membrane permeability to Na+

Seeman, Philip; Kwant, W.O.; Goldberg, M A; Chau-Wong, M.

doi:10.1016/0005-2736(71)90035-6

Cited by 34 publications

(3 citation statements)

References 32 publications

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“…Previous investigations have shown that local anesthetics expand the erythrocyte membrane (Seeman, 1966) and reduce both active and passive cation fluxes (Andersen, 1968). They, furthermore, reduce the enhancement of passive sodium fluxes caused by butanol (Burt & Green, 1971) or caused by Ca ++ in both erythrocytes (Seeman, Kwant, Goldberg & Chau-Wong, 1971) and phosphatidylserine vesicles (Papahadjopoulos, 1970). These findings appear to be in accord with the evidence that the hydrophobic tail of these molecules can become incorporated into cell membranes (Cerbdn, 1972) thereby causing expansion, and the polar end of these molecules when positively charged can contribute to the net surface charge.…”

supporting

confidence: 67%

Effect of local anesthetics on chloride transport in erythrocytes

1975

J. Membrain Biol.

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The self-exchange of chloride isotopes across the human erythrocyte membrane was inhibited by tetracaine, benzocaine, and lidocaine. The inhibition by tetracaine was increased at higher pH values, but was not exclusively due to the uncharged form of tetracaine. The inhibition was effective within 5 seconds, was reversible, was non competitive with chloride ions, and was not reversed by calcium ions. These findings indicate that local anesthetics react with the erythrocyte chloride carrier at a site separate from the chloride site and cause inhibition of anion transport by a specific mechanism not involving changes in the surface charge density on the erythrocyte membrane.

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supporting

confidence: 67%

Effect of local anesthetics on chloride transport in erythrocytes

1975

J. Membrain Biol.

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“…According to this theory, chemical agents, such as ethanol, adsorb to the hydrophobic regions of excitable membranes and cause expansion of the hydrophobic regions of membrane proteins; as a result channels for Na+ and K+ are restricted. In support of this theory are observations in acute experiments of decreased passive exchange of Na in frog sartorius muscle (Seeman et al, 1971) and decreased resting membrane conductance (i.e., in increased Em), in squid axon (Armstrong and Binstock, 1964), and spinal cord neurons in culture (Gruol, 1980). If the neuronal cell membrane, during chronic exposure to ethanol, adapted in some way to the restriction of Na+ and K+ channels so as to restore normal permeability, then upon return to ethanol-free medium, the membrane would be in an "unadapted" state and resting conductance would ETHANOL EFFECTS ON NEURONS 389 be too high (i.e., € 2 , too low).…”

Section: E F F E C T Of Ethanol On E M Pmentioning

confidence: 85%

Effect of chronic ethanol exposure on the electric membrane properties of DRG neurons in cell culture

Scott

Edwards

1981

J. Neurobiol.

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Neural cell cultures of adult mouse dorsal root ganglia were utilized to investigate the effects of chronic ethanol exposure on neuronal electric membrane properties (EMP). After 12 days of exposure to various ethanol concentrations, the EMP of the neurons were determined in ethanol-free medium. Significant changes in a number of EMP were observed. Of particular physiological significance were decreased specific membrane resistance, increased specific membrane capacitance, relatively little change in membrane time constant, and increased electrical excitability. Various features of the action potential were also affected, e.g., reduced overshoot, afterhyperpolarization, and rate of rise. In preliminary experiments, EMP were determined at varying periods after the cultures had been withdrawn from ethanol medium and maintained in ethanol-free medium. These results indicated that the altered EMP persisted as long as one (Cm) to two (Rm) weeks after ethanol withdrawal. A possible mechanism for these ethanol-induced changes in EMP was suggested, utilizing the membrane expansion theory of anesthesia. Because of few previous reports demonstrating significant electrophysiological effects of ethanol at pharmacological concentrations, the neural cell culture system provides a useful new experimental model for studying the action of chronic ethanol exposure on neuronal EMP and the physical basis of the tolerance and withdrawal phenomena found in alcoholism and addiction in general. After being maintained for 12 days in culture media containing various concentrations of ethanol, non-neuronal cell survival was observed to have decreased in an approximately linear manner with increasing ethanol levels. By contrast, neuron survival was not affected until ethanol concentrations greater than 0.34 g % were used. This decreased cell survival due to chronic exposure to physiological levels of ethanol has not been reported previously. Neural cell cultures may therefore be useful for investigating the cellular pathology of chronic alcoholism and fetal alcohol syndrome.

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“…(1) bind to microsomaI [10, 26, 4I], lysosomal [591, mitochondrial [59], erythrocytic [34,59,69] or synthetic [34,106] membranes and form stable complexes with phospholipids [73]; (2) inhibit under certain experimental conditions several microsomal enzyme systems involved in the biotransformation [4,40,47,58,63,64,89,90,109,110,115,116,123,129,131] or conjugation [22,35,46,58] of drugs and in the biosynthesis of cholesterol [51,91]; (3) stabilize the lysosomal [43,59,134] and the erythrocytic [38,59,105] membrane, 'immobilize' and solubilize spin-labelled proteins of synaptosomal membranes [71] and prevent mitochondrial swelling [38,59]; (4) (5) interfere with the 'amine pump' [17,18,39,77,78,85,…”

Section: Figures 5 Andmentioning

confidence: 99%

Ultrastructural and biochemical study of the action of benzoctamine and maprotiline on the rat liver

et al. 1974

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The changes induced in the liver epithelium of male rats by two dibenzobicyclo octadiene analogues, maprotiline and benzoetamine, were compared. Maprotiline at high dose levels produced induction of microsomal membranes and of constituent enzymes of the endoplasmie reticulum (ER), preceded by the appearance of altered peribiliary structures, part of which showed the morphological aspect of myeloid bodies. These particles, which appeared to develop at the expense of peribiliary dense bodies, were considered to be of a lysosomal nature by virtue of their acid phosphatase activity. All the hepatic changes induced by maprotiline proved to be reversible upon cessation of treatment. Since changes similar to those caused by maprotiline were also induced by amitriptyline, imipramine and chlorpromazine, they may conceivably be produced nonspecifically by lipophilic bases. Benzoctamine, being of a less basic nature, was found to induce reversible hypertrophy of the SER only.

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The effects of ethanol and chlorpromazine on the passive membrane permeability to Na+

Cited by 34 publications

References 32 publications

Effect of local anesthetics on chloride transport in erythrocytes

Effect of local anesthetics on chloride transport in erythrocytes

Effect of chronic ethanol exposure on the electric membrane properties of DRG neurons in cell culture

Ultrastructural and biochemical study of the action of benzoctamine and maprotiline on the rat liver

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