Effect of activators and blockers of ligand-regulated ion channels on the activity of the Cl-stimulated Mg2+-ATPase of the plasma membrane fraction from bream (Abramis brama L.) brain.
Effects of GABA, glycine, acetylcholine, and glutamate (agonists of the GABAa/benzodiazepine, glycine, choline, and glutamate receptors, respectively) at concentrations in the range 10(-8)-10(-4) M on the activity of "basal" Mg(2+)-ATPase of the plasma membrane fraction from bream brain and on its activation by Cl(-) were investigated. GABA and glycine activated "basal" Mg(2+)-ATPase activity and suppressed its activation by Cl(-). Acetylcholine and glutamate activated "basal" Mg(2+)-ATPase to a lesser extent and did not suppress the activation of the enzyme by Cl(-). The activation of "basal" Mg(2+)-ATPase by neuromediators was decreased by blockers of the corresponding receptors (picrotoxin, strychnine, benztropine mesylate, and D-2-amino-5-phosphonovaleric acid). In addition, picrotoxin and strychnine eliminated the inhibiting effect of GABA and glycine, respectively, on the Cl(-)-stimulated Mg(2+)-ATPase activity. Agonists of the GABAa/benzodiazepine receptor--phenazepam (10(-8)-10(-4) M) and pentobarbital (10(-6)-10(-3) M)--activated the "basal" Mg(2+)-ATPase activity and decreased the Cl(-)-stimulated Mg(2+)-ATPase activity. The dependence of both enzyme activities on ligand concentration is bell-shaped. Moreover, phenazepam and pentobarbital increased the "basal" Mg(2+)-ATPase activity in the presence of 10(-7) M GABA and did not influence it in the presence of 10(-4) M GABA and 10(-6) M glycine. The data suggest that in the fish brain membranes the Cl(-)-stimulated Mg(2+)-ATPase interacts with GABAa/benzodiazepine and glycine receptors but not with m-choline and glutamate receptors.
Menzikov
S A
SA
Papanin Institute of Biology of Inland Waters, Russian Academy of Sciences, Borok, Yaroslavl Region, 152742 Russia. sam@ibiw.yaroslavl.ru
Menzikova
O V
OV
D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000201:enzymology; D017301:Ca(2+) Mg(2+)-ATPase / Q000378:metabolism*; D002462:Cell Membrane / Q000187:drug effects / Q000201:enzymology; D002794:Choline / Q000494:pharmacology*; D004789:Enzyme Activation; D020536:Enzyme Activators / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology*; D058787:GABA-A Receptor Antagonists; D007473:Ion Channels / Q000502:physiology*; D008024:Ligands; D011963:Receptors, GABA-A / Q000378:metabolism; D017470:Receptors, Glutamate / Q000378:metabolism; D018009:Receptors, Glycine / Q000037:antagonists & inhibitors / Q000378:metabolism; D021541:Sea Bream
D020536:Enzyme Activators; D004791:Enzyme Inhibitors; D058787:GABA-A Receptor Antagonists; D007473:Ion Channels; D008024:Ligands; D011963:Receptors, GABA-A; D017470:Receptors, Glutamate; D018009:Receptors, Glycine; D017301:Ca(2+) Mg(2+)-ATPase; D002794:Choline