Spontaneous and evoked release of [3H]taurine from a P2 subcellular fraction of the rat retina.
The effects of spontaneous and evoked [3H]taurine release from a P2 fraction prepared from rat retinas were studied. The P2 fraction was preloaded with [3H]taurine under conditions of high-affinity uptake and then examined for [3H]taurine efflux utilizing superfusion techniques. Exposure of the P2 fraction to high K+ (56 mM) evoked a Ca(2+)-independent release of [3H]taurine. Li+ (56 mM) and veratridine (100 microM) had significantly less effect (8-15% and 15-30%, respectively) on releasing [3H]taurine compared to the K(+)-evoked release. 4-Aminopyridine (1 mM) had no effect on the release of [3H]taurine. The spontaneous release of [3H]taurine was also Ca(2+)-independent. When Na+ was omitted from the incubation medium K(+)-evoked [3H]taurine release was inhibited by approximately 40% at the first 5 minute depolarization period but was not affected at a second subsequent 5 minute depolarization period. The spontaneous release of [3H]taurine was inhibited by 60% in the absence of Na+. Substitution of Br- for Cl- had no effect on the release of either spontaneous or K(+)-evoked [3H]taurine release. However, substitution of the Cl- with acetate, isethionate, or gluconate decreased K(+)-evoked [3H]taurine release. Addition of taurine to the superfusion medium (homoexchange) resulted in no significant increase in [3H]taurine efflux. The taurine-transport inhibitor guanidinoethanesulfonic acid increased the spontaneous release of [3H]taurine by approximately 40%. These results suggest that the taurine release of [3H]taurine is not simply a reversal of the carrier-mediated uptake system. It also appears that taurine is not released from vesicles within the synaptosomes but does not rule out the possibility that taurine is a neurotransmitter. The data involving chloride substitution with permeant and impermeant anions support the concept that the major portion of [3H]taurine release is due to an osmoregulatory action of taurine while depolarization accounts for only a small portion of [3H]taurine release.
Lombardini
J B
JB
Department of Pharmacology, Texas Tech University Health Sciences Center, Lubbock 79430.
D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002712:Chlorides / Q000494:pharmacology; D008094:Lithium / Q000494:pharmacology; D010477:Perfusion; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D012160:Retina / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D012964:Sodium / Q000494:pharmacology; D013347:Subcellular Fractions / Q000378:metabolism; D013654:Taurine / Q000031:analogs & derivatives / Q000378:metabolism* / Q000494:pharmacology; D014316:Tritium; D014701:Veratridine / Q000494:pharmacology
D002712:Chlorides; D014316:Tritium; D013654:Taurine; C009558:taurocyamine; D014701:Veratridine; D008094:Lithium; D012964:Sodium; D015761:4-Aminopyridine; D011188:Potassium; D002118:Calcium