Hollins C, Stone T W
Br J Pharmacol. 1980 May;69(1):107-12. doi: 10.1111/j.1476-5381.1980.tb10888.x.
1 The effect of purine compounds on the potassium-evoked release of 14C-labelled gamma-aminobutyric acid (GABA) has been studied in 400 micrometers slices of rat cerebral cortex in vitro. 2 Adenosine and adenosine 5' monophosphate (AMP) inhibited the release of GABA at 10(-5) to 10(-3) M. Adenosine triphosphate (ATP) produced a significant inhibition of release only at 10(-3) M. 3 Theophylline 10(-4) or 10(-3) M reduced the inhibitory effect of adenosine, but did not change basal release of GABA. 4 Dipyridamole 10(-5) M itself reduced evoked GABA release, but did not prevent the inhibitory effect of adenosine, implying that adenosine was acting at an extracellularly directed receptor. 5 Calcium removal or antagonism by verapamil reduced the evoked release of GABA, but adenosine did not produce any further reduction of the calcium-independent release. This may indicate that the inhibitory effect of adenosine on GABA release results from interference with calcium influx or availability within the terminals.
嘌呤化合物对体外培养的400微米厚大鼠大脑皮质切片中钾离子诱发的14C标记γ-氨基丁酸(GABA)释放的影响已被研究。
腺苷和5'-磷酸腺苷(AMP)在10^(-5)至10^(-3)M浓度下抑制GABA的释放。三磷酸腺苷(ATP)仅在10^(-3)M时对释放产生显著抑制作用。
10^(-4)或10^(-3)M的茶碱可降低腺苷的抑制作用,但不改变GABA的基础释放量。
10^(-5)M的双嘧达莫本身可降低诱发的GABA释放,但不能阻止腺苷的抑制作用,这表明腺苷作用于细胞外定向受体。
去除钙离子或用维拉帕米拮抗可降低诱发的GABA释放,但腺苷不会使非钙依赖性释放进一步降低。这可能表明腺苷对GABA释放的抑制作用是由于干扰了神经末梢内的钙离子内流或可利用性。