Gamma Aminobutyric acid uptake, release, and effect on 36Cl--influx in bovine pineal gland.

Abstract

Two apparent affinities for Na+-dependent, 3H-GABA uptake were found in bovine pineal fragments in vitro i.e., a high affinity uptake (Km = 37 +/- 5 microM) and a low affinity uptake (Km = 435 +/- 50 microM). GABA or the neuronal and glial GABA uptake inhibitor nipecotic acid was significantly more effective than the inhibitor of the GABA glial uptake beta-alanine to decrease pineal 3H-GABA uptake. High K+ concentration release 3H-GABA in superfused bovine pineals, no differences in 3H-GABA release among fragments taken from medial, proximal or distal pineal regions being apparent. Superfusion of pineal fragments in the absence of Ca2+ but in the presence of EGTA, Mg2+ or verapamil decreased significantly 3H-GABA release induced by K+. In every case a Ca2+-independent pineal GABA release was found. Preincubation with GABA or nipecotic acid, but not with beta-alanine, blunted subsequent 3H-GABA release. GABA increased 36Cl--influx in pineal homogenates, an effect blocked by picrotoxin. Incubation of pineal homogenates in the presence of aminooxyacetic acid decreased Vmax of glutamic acid decarboxylase, without modifying its Km. These results are compatible with a transmitter or modulator role of GABA in bovine pineal gland.