Proctor W R, Dunwiddie T V
Department of Pharmacology, University of Colorado Health Sciences Center, Denver 80262.
Brain Res. 1987 Nov 17;426(1):187-90. doi: 10.1016/0006-8993(87)90441-0.
The mechanisms underlying the depressant effect of adenosine on excitatory synaptic transmission were studied in rat hippocampus in vitro. The relative contribution of direct effects of adenosine upon CA1 pyramidal neurons (hyperpolarization, increased conductance) was evaluated by comparing the effects of superfused adenosine on EPSP amplitude, and on depolarizing responses to local application of glutamate. Adenosine depressed synaptic EPSPs to a greater extent than glutamate responses in 30 out of 32 cases, and its effects were independent of the site of glutamate application (somatic vs dendritic). Thus, the postsynaptic effects of adenosine, including a possible dendritic conductance that would be undetectable with somatic recordings, can only partially account for the depression of synaptic potentials observed with adenosine.
在体外培养的大鼠海马体中研究了腺苷对兴奋性突触传递的抑制作用机制。通过比较灌流腺苷对兴奋性突触后电位（EPSP）幅度以及对局部应用谷氨酸的去极化反应的影响，评估了腺苷对CA1锥体神经元的直接作用（超极化、电导增加）的相对贡献。在32例中有30例，腺苷对突触EPSP的抑制程度大于对谷氨酸反应的抑制程度，并且其作用与谷氨酸应用部位（体细胞与树突）无关。因此，腺苷的突触后效应，包括可能无法通过体细胞记录检测到的树突电导，只能部分解释腺苷引起的突触电位抑制。
