Action of amino acids and convulsants on cerebellar spontaneous action potentials in vitro: effects of deprivation of C1-, K+ of Na+.
(1) The inhibition of spontaneous action potentials in guinea pig cerebellar cortex slices by GABA, glycine, taurine and beta-alanine is maintained when C1- in the superfusion medium is almost completely replaced by NO3- or I-('permeant' anion), but the inhibition decreases in magnitude with repeated application of the amino acid. Replacement of C1- by sulfate or isethionate ('impermeant' anion) causes a conversion of inhibition by these amino acids to excitation. The initial excitation which is sometimes seen with these inhibitory amino acids in high C1- media is abolished when C1- is replaced by either permeant or impermeant anions. (2) Reduction of K+ in the medium causes an increase of inhibition by the inhibitory amino acids in the presence of high C1- and reduction of excitation when C1- is replaced by impermeant anion. (3) Excitation by GABA in impermeant anion (low C1-) media  is unaffected by reduction of Na+ in the media by 50% but excitations by glycine, taurine, beta-alanine and L-glutamate are greatly reduced. (4). Excitation by GABA in impermeant anion (low C1-) media is abolished by picrotoxin and bicuculline which both suppress inhibition by GABA in a high C1- medium. Strychnine suppresses the effects of glycine, taurine and beta-alanine in either a low or high C1- medium. Bicuculline blocks the inhibitory effect of these three amino acids in a high C1- medium but does not affect their excitatory effects in a low C1- medium. (5) These results are consistent with the hypothesis that the inhibitory amino acids, GABA, glycine, taurine and beta-alanine, cause inhibition via increase of C1- (and perhaps K+) permeability and that glycine, taurine and beta-alanine also interact with strychnine-sensitive receptors mediating (perhaps indirectly) increased permeability to Na+ and, therefore, excitation in low C1- media.
D000200:Action Potentials / Q000187:drug effects*; D000409:Alanine / Q000494:pharmacology; D000596:Amino Acids / Q000494:pharmacology*; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002531:Cerebellum / Q000187:drug effects* / Q000378:metabolism; D002712:Chlorides / Q000378:metabolism; D005998:Glycine / Q000494:pharmacology; D006168:Guinea Pigs; D007454:Iodides / Q000494:pharmacology; D007513:Isethionic Acid / Q000494:pharmacology; D009566:Nitrates / Q000494:pharmacology; D010852:Picrotoxin / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D012964:Sodium / Q000378:metabolism; D013331:Strychnine / Q000494:pharmacology; D013431:Sulfates / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D000409:Alanine; D000596:Amino Acids; D001640:Bicuculline; D002712:Chlorides; D005998:Glycine; D007454:Iodides; D007513:Isethionic Acid; D009566:Nitrates; D010852:Picrotoxin; D011188:Potassium; D012964:Sodium; D013331:Strychnine; D013431:Sulfates; D005680:gamma-Aminobutyric Acid