Randoll L A, Wilson W R, Weaver M S, Spuhler-Phillips K, Leslie S W
Division of Pharmacology and Toxicology, College of Pharmacy, University of Texas at Austin 78712-1074, USA.
Alcohol Clin Exp Res. 1996 Apr;20(2):197-200. doi: 10.1111/j.1530-0277.1996.tb01629.x.
This study compared N-methyl-D-aspartate (NMDA)-stimulated increases in intracellular calcium in fura-2-loaded neurons dissociated from newborn rat brainstem (EC50 in microM; 6.4), cerebellum (9.5), forebrain (6.3), and hippocampus (10.6). Ethanol inhibition of the response to 25 microM NMDA differed among the regions. The NMDA response in hippocampus was inhibited by 20 mM ethanol; cortex and cerebellum responses were inhibited by 80 mM ethanol, and no inhibition was seen in the brainstem. Addition of glycine (15 microM) failed to attenuate ethanol inhibition of the NMDA response. These results demonstrate that ethanol inhibition of NMDA-stimulated responses varies according to brain region. In contrast to previous findings from this laboratory using dissociated neurons from whole brain, the addition of glycine did not reverse the inhibitory effects of ethanol on NMDA-stimulated responses.
本研究比较了N-甲基-D-天冬氨酸(NMDA)刺激下,从新生大鼠脑干(半数有效浓度[EC50],以微摩尔计;6.4)、小脑(9.5)、前脑(6.3)和海马体(10.6)分离出的经fura-2负载的神经元内钙离子的增加情况。乙醇对25微摩尔NMDA反应的抑制作用在不同脑区有所差异。海马体中NMDA反应受到20毫摩尔乙醇的抑制;皮层和小脑的反应受到80毫摩尔乙醇的抑制,而在脑干中未观察到抑制作用。添加甘氨酸(15微摩尔)未能减弱乙醇对NMDA反应的抑制作用。这些结果表明,乙醇对NMDA刺激反应的抑制作用因脑区而异。与本实验室之前使用全脑分离神经元的研究结果相反,添加甘氨酸并未逆转乙醇对NMDA刺激反应的抑制作用。