Muscimol potentiation of acidic amino acid release from cerebellar synaptosomes is chloride dependent.
In previous studies we have shown that the depolarization-induced release of preaccumulated acidic amino acids and newly synthesized glutamate from cerebellar synaptosomal preparations is potentiated by gamma-aminobutyric acid (GABA) agonists through a GABAergic presynaptic mechanism. Here we report a systematic analysis of the ionic requirements of the potentiating effect of muscimol on the high K+-evoked release of D-[3H]aspartate. Our studies show that: Ca2+, Na+, and Mg2+ are not required for muscimol to exert its effect; a depolarizing concentration of K+ is a necessary, but not sufficient, condition to observe the presynaptic effect in question; and a minimal Cl- concentration (50-70 mM) is also required. A possible model based on these findings is proposed.
D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism*; D002531:Cerebellum / Q000378:metabolism*; D002712:Chlorides / Q000494:pharmacology*; D004357:Drug Synergism; D007477:Ions; D007700:Kinetics; D008297:Male; D009118:Muscimol / Q000494:pharmacology*; D009994:Osmolar Concentration; D010080:Oxazoles / Q000494:pharmacology*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013574:Synaptosomes / Q000187:drug effects / Q000378:metabolism*
D002712:Chlorides; D007477:Ions; D010080:Oxazoles; D009118:Muscimol; D001224:Aspartic Acid; D011188:Potassium