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Ethanol‐induced Inhibition of Mouse Brain Adenosine Triphosphatase Activities: Lack of Interaction with Norepinephrine in Vitro
Author(s) -
Syapin Peter J.,
Alkana Ronald L
Publication year - 1986
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1986.tb05159.x
Subject(s) - forebrain , norepinephrine , atpase , chemistry , medicine , endocrinology , in vitro , enzyme , biology , dopamine , biochemistry , central nervous system
The In vitro effects of ethanoi on C57BL/6J mouse forebrain ATPase activities were investigated in the presence and absence of norepinephrine. Three enzyme activities (Na + K‐ATPase, Mg‐ATPase, and low affinity Ca‐ATPase) were studied in forebrain homogenates using a coiorimetric assay. The effect of norepinephrine on ethanoi inhibition of Sprague‐Oawley rat brain Na + K‐ATPase activity was examined in selected experiments for direct comparison with the results obtained using mouse brain. Ethanoi (250–2000 HIM) inhibited all ATPase activities in a concentration‐dependent manner. In each case the IC50 was well beyond what would be a lethal concentration in vivo. Ethanoi inhibition of mouse forebrain Na + K‐ATPase activity was competitive with regards to K* ion concentration, but was uncompetitive for inhibition of Mg‐ATPase and Ca‐ATPase activities. Norepinephrine (0.1 m) did not sensitize mouse brain Na + K‐ATPase activity to ethanoMnduced inhibition. In contrast, norepinephrine sensitized rat brain Na + K‐ATPase to ethanoi inhibition when tested simultaneously with mouse brain under identical conditions. These results cannot be explained by differences in assay conditions and suggest that the interaction between norepinephrine and ethanoi inhibition of Na + K‐ATPase activity may be species specific. Norepinephrine alone stimulated mouse and rat brain Na + K‐ATPase activity when assayed in imidazole buffer, but not when assayed in tris buffer. Furthermore, 0.1 mM norepinephrine slightly antagonized the inhibitory effect of ethanoi on mouse brain Mg‐ATPase activity, but did not affect ethanol‐induced inhtottion of Ca‐ATPase activity. The high ethanoi concentrations (250–2000 mM) needed to induce in vitro inhibition of mouse brain ATPase activities suggest that ATPase inhibition is not a critical event mediating ethanol‐induced behavioral effects, however further experiments are needed before conclusions can be drawn.