Russell V A, Lamm M C, Taljaard J J
Department of Chemical Pathology, University of Stellenbosch, Tygerberg Hospital, Republic of South Africa.
Neurochem Res. 1988 May;13(5):487-92. doi: 10.1007/BF01268885.
Ethanol (10-200 mM) transiently increased tritium overflow from superfused rat nucleus accumbens slices previously incubated with [3H]dopamine (DA) and [14C]choline. The effect was greater in striatal tissue and did not appear to be a non-specific membrane effect since [14C]acetylcholine (ACh) release was not affected. Lack of antagonism by picrotoxin suggested that gamma-aminobutyric acid (GABA) receptors were not involved. Calcium was not a requirement and the DA uptake blocker, nomifensine, was without effect. Ethanol appeared to be causing [3H]DA release into the cytoplasm. K+ -stimulated release of [3H]DA and [14C]ACh from nucleus accumbens and striatal slices was not affected. Clonidine-mediated inhibition of the K+-evoked release of [3H]DA remained unaltered. Ethanol attenuated the isoproterenol-induced enhancement of [3H]DA release. Ethanol therefore appeared to interact with components of the DA terminal causing a transient increase in the release of neurotransmitter without impairing K+-evoked release but apparently interfering with the isoproterenol-induced effect.
乙醇（10 - 200 mM）可使预先用[3H]多巴胺（DA）和[14C]胆碱孵育的大鼠伏隔核灌流切片中的氚溢出量短暂增加。这种效应在纹状体组织中更明显，且似乎不是非特异性膜效应，因为[14C]乙酰胆碱（ACh）的释放未受影响。苦味毒素无拮抗作用表明γ-氨基丁酸（GABA）受体未参与其中。钙并非必需条件，多巴胺摄取阻滞剂诺米芬辛也无作用。乙醇似乎促使[3H]DA释放到细胞质中。K⁺刺激伏隔核和纹状体切片释放[3H]DA和[14C]ACh不受影响。可乐定介导的对K⁺诱发的[3H]DA释放的抑制作用保持不变。乙醇减弱了异丙肾上腺素诱导的[3H]DA释放增强。因此，乙醇似乎与DA终末的成分相互作用，导致神经递质释放短暂增加，而不损害K⁺诱发的释放，但显然干扰了异丙肾上腺素诱导的效应。
