Further studies on the role of calcium in the regulation of glutamate decarboxylase activity in brain slices.
[3H]GABA synthesis in brain slices was used as a model to study the role of Ca2+ in the regulation of GAD activity. Experimental conditions were chosen to increase and decrease the flux of Ca2+ and to promote the increase in free intracellular Ca2+. The blockade of electron transport and the inhibition of oxidative phosphorylation in the slices inhibited [3H]GABA synthesis. High K+ depolarization stimulated [3H]GABA synthesis and this effect was not blocked by lidocaine, trifluoperazine, or verapamil, but the stimulation was blocked by the intracellular Ca2+ antagonist TMB-8. The data do not differentiate between the relative contributions of extra- and intracellular Ca2+ but reflect that GAD activity is modulated by a dynamic balance between these two compartments as well as between stored and free Ca2+ within the cells.
D019297:2,4-Dinitrophenol; D000818:Animals; D000968:Antimycin A / Q000494:pharmacology; D001921:Brain / Q000201:enzymology*; D002118:Calcium / Q000502:physiology*; D002262:Carboxy-Lyases / Q000378:metabolism*; D003342:Corpus Striatum / Q000378:metabolism; D004140:Dinitrophenols / Q000494:pharmacology; D005968:Glutamate Decarboxylase / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D011188:Potassium / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D014268:Trifluoperazine / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000096:biosynthesis
D004140:Dinitrophenols; D014268:Trifluoperazine; D005680:gamma-Aminobutyric Acid; D000968:Antimycin A; D014700:Verapamil; D002262:Carboxy-Lyases; D005968:Glutamate Decarboxylase; D019297:2,4-Dinitrophenol; D011188:Potassium; D002118:Calcium