Spencer N J, Bywater R A, Holman M E, Taylor G S
Department of Physiology, Monash University, Clayton, Victoria, Australia.
J Auton Nerv Syst. 1998 Apr 30;69(2-3):115-21. doi: 10.1016/s0165-1838(98)00012-5.
Intracellular microelectrodes were used to record spontaneous and evoked inhibitory junction potentials (IJPs) from the circular muscle layer of an in vitro preparation of whole mouse colon. Membrane potential recordings were made from cells of the mid to distal region of colon at 36 +/- 1 degrees C in a modified Krebs' solution that contained atropine (1 microM) and nifedipine (1-2 microM). Spontaneously occurring hyperpolarisations of irregular amplitude and frequency (range: up to 20 mV and 2 Hz) were recorded that were resistant to N(G)-nitro-L-arginine (NOLA, 100 microM), but were abolished by tetrodotoxin (TTX, 1.6 microM) or apamin (250 nM). These were considered to be spontaneous IJPs as a consequence of activity in inhibitory motor neurons. Single electrical stimuli (0.6 ms, 15 V), elicited a fast IJP, whose time course could be superimposed on spontaneous IJPs of similar amplitude. The amplitude of evoked IJPs was not depressed by NOLA (100 microM). However, in NOLA (100 microM), further addition of apamin (250 nM) significantly depressed the amplitudes of the evoked IJPs by 44%. NOLA- and apamin-resistant evoked IJPs were abolished by TTX (1.6 microM). It is suggested, that in the circular muscle layer of mouse colon, NO does not mediate the fast hyperpolarisations associated with spontaneous or evoked IJPs. Apamin abolished spontaneous IJPs, but electrical stimuli evoked an IJP with apamin-sensitive and resistant components both of which were non-nitrergic in origin.
使用细胞内微电极记录来自全小鼠结肠体外制备物环形肌层的自发性和诱发性抑制性接头电位（IJP）。在含有阿托品（1μM）和硝苯地平（1 - 2μM）的改良克雷布斯溶液中，于36±1℃从结肠中至远端区域的细胞进行膜电位记录。记录到了幅度和频率不规则的自发性超极化（范围：高达20 mV和2 Hz），其对N（G）-硝基-L-精氨酸（NOLA，100μM）有抗性，但被河豚毒素（TTX，1.6μM）或蜂毒明肽（250 nM）消除。这些被认为是抑制性运动神经元活动导致的自发性IJP。单个电刺激（0.6 ms，15 V）引发快速IJP，其时间进程可叠加在类似幅度的自发性IJP上。诱发性IJP的幅度不受NOLA（100μM）抑制。然而，在NOLA（100μM）中，进一步添加蜂毒明肽（250 nM）可使诱发性IJP的幅度显著降低44%。NOLA和蜂毒明肽抗性的诱发性IJP被TTX（1.6μM）消除。提示在小鼠结肠环形肌层中，一氧化氮不介导与自发性或诱发性IJP相关的快速超极化。蜂毒明肽消除自发性IJP，但电刺激引发的IJP具有蜂毒明肽敏感和抗性成分，两者均起源于非硝基能。
