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The uptake and release of γ-[³H]-aminobutyric acid ([³H]-GABA) by the median eminence and the neurointermediate lobe of the pituitary was investigated using sucrose homogenates as crude synaptosomal preparations. Uptake in both areas showed predominantly neuronal specificity and similar K_m values, but the median eminence had a considerably greater V_max value. Release of [³H]-GABA could be stimulated by elevated K⁺ concentrations, in a Ca²⁺-dependent manner. Stimulated release was reduced by muscimol, implying the existence of presynaptic autoreceptors in both areas. A number of other transmitters and peptide hormones were demonstrated to have no effect on stimulated release of [³H] GABA in either area.

Calcium-mobilizing receptors appear to induce calcium movements from both intracellular and extracellular sites.' The mechanism of the Ca2+ influx component remains enigmatic, being probably independent from voltage-sensitive Caz+ channels because it occurs in both excitable and nonexcitable cell types. Several hypotheses for the mechanism have been proposed, including actions of inositol tetrakis-and tris-phosphates, Ca2+-activated Ca2+ channels, and the Na+ /Ca2+One further possibility is that the concomitant activation of protein kinase C (PKC) by such receptors may have a role in signaling Ca2+ influx.Luteinizing hormone-releasing hormone ( LHRH) and thyrotrophin-releasing hormone (TRH) both act through this class of receptor, causing calcium mobilization and phosphoinositide hydrolysis. The Ca-influx processes activated by these hormone receptors in anterior pituitary tissue can be measured by a rapid "Ca2+ influx assay, involving quenching, filtration, and washing with EGTA-containing medium.' The 4sCa2+ influx induced by LHRH, TRH, or K + was maximal by 30 seconds and was concentration dependent, with peak increases over basal "Ca2+ accumulation of 83 2 8% (100 nM LHRH), 162 * 14% (300 nM TRH), and 232 2 30% (60 mM

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