Saito N, Taniyama K, Tanaka C
Naunyn Schmiedebergs Arch Pharmacol. 1984 May;326(1):45-8. doi: 10.1007/BF00518777.
We investigated the effect of GABA on the spontaneous efflux of 3H-acetylcholine (ACh) from the isolated guinea pig gallbladder loaded with 3H-choline. Application of GABA (10(-5) M) caused a significant increase in the fractional rate of tritium efflux. This GABA-evoked efflux of ACh was inhibited by the perfusion of tetrodotoxin (10(-6) M) and Ca-free medium. Nipecotic acid (10(-4) M) did not affect the GABA-evoked release of ACh, indicating that ACh was not released by the entry of GABA into cholinergic nerve terminals. Bicuculline (10(-6) M) and furosemide (10(-6) M), the chloride ion channel blocker, inhibited the GABA-evoked ACh release. The application of muscimol (10(-5) M), but not baclofen (10(-5) M) also produced an increase in the fractional rate of ACh release. Thus, the GABA receptors involved in the increase of ACh release are bicuculline-sensitive. The GABA-evoked release of ACh was not altered by the perfusion with hexamethonium (10(-5) M), thus indicating the presence of GABA receptors on the postganglionic cholinergic neurons. These findings suggest that bicuculline-sensitive GABA receptors probably coupled to a Cl- ionophore are present on postganglionic cholinergic neurons and are involved in the increase of ACh release in guinea pig gallbladder.
我们研究了γ-氨基丁酸（GABA）对装载有3H-胆碱的离体豚鼠胆囊中3H-乙酰胆碱（ACh）自发流出的影响。应用GABA（10^(-5) M）导致氚流出分数率显著增加。这种GABA诱发的ACh流出被河豚毒素（10^(-6) M）灌注和无钙培养基抑制。尼克酸（10^(-4) M）不影响GABA诱发的ACh释放，表明ACh不是通过GABA进入胆碱能神经末梢而释放的。荷包牡丹碱（10^(-6) M）和氯离子通道阻滞剂速尿（10^(-6) M）抑制GABA诱发的ACh释放。应用蝇蕈醇（10^(-5) M）而非巴氯芬（10^(-5) M）也使ACh释放分数率增加。因此，参与ACh释放增加的GABA受体对荷包牡丹碱敏感。用六甲铵（10^(-5) M）灌注不改变GABA诱发的ACh释放，从而表明节后胆碱能神经元上存在GABA受体。这些发现提示，对荷包牡丹碱敏感的GABA受体可能与氯离子载体偶联，存在于节后胆碱能神经元上，并参与豚鼠胆囊中ACh释放的增加。
