Haas H L, Greene R W
Pflugers Arch. 1984 Nov;402(3):244-7. doi: 10.1007/BF00585506.
Adenosine added to the perfusion fluid of rat hippocampal slices at 10 mumol X l-1 enhanced long lasting afterhyperpolarizations after single action potentials, bursts of action potentials or calcium spikes. Accommodation of firing during a depolarizing pulse was potentiated. An increase in calcium dependent potassium conductance is likely to mediate these effects. Adenosine at 50 mumol X l-1 induced a hyperpolarization accompanied by a reduction in input resistance. The hyperpolarization could be reversed at -85 mV. In TTX and TTX-barium treated slices the amplitude of the slow spike was decreased. This may result from a shunting of inward current in the dendrites due to an adenosine induced increase in potassium conductance. It is suggested that adenosine reduces pre- and postsynaptic excitatory signals principally by enhancing one or more potassium conductances. This effect is a powerful means for modulation of neuronal excitability and synaptic efficacy and can explain the antiepileptic activity of adenosine.
向大鼠海马切片灌注液中添加10微摩尔/升的腺苷，可增强单动作电位、动作电位爆发或钙峰后的长时程超极化后电位。去极化脉冲期间的放电适应性增强。钙依赖性钾电导的增加可能介导了这些效应。50微摩尔/升的腺苷诱导超极化并伴有输入电阻降低。该超极化在-85毫伏时可逆转。在经河豚毒素（TTX）和TTX-钡处理的切片中，慢波峰的幅度减小。这可能是由于腺苷诱导的钾电导增加导致树突内向电流分流所致。提示腺苷主要通过增强一种或多种钾电导来降低突触前和突触后兴奋性信号。这种效应是调节神经元兴奋性和突触效能的有力手段，并且可以解释腺苷的抗癫痫活性。
