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 May 28;70(1-2):10-4. doi: 10.1016/s0165-1838(98)00045-9.
Intracellular electrophysiological techniques were used to record the spontaneous myoelectric activity in the circular muscle layer of an in vitro preparation of whole mouse colon. In 34 out of 58 preparations, spontaneous depolarisations (myoelectric complexes, MCs) were recorded cyclically, about every 4 min. In these preparations, apamin (250 nM) and NG-nitro-L-arginine (NOLA, 100 microM) depolarised the membrane potential between MCs by 8 mV or 13 mV, respectively. Tetrodotoxin (1.6 microM) abolished MCs and also induced depolarisation (17 mV). In the remaining 24 preparations, MCs were not recorded and the membrane potential was significantly depolarised compared to the membrane potential between MCs. NOLA (100 microM), apamin (250 nM) and tetrodotoxin (1.6 microM) were without significant effect on membrane potential. It is suggested that in preparations that exhibit MC cycling, membrane potential between MCs is maintained in a state of tonic inhibition, predominantly mediated by nitrergic mechanisms generated via spontaneously active inhibitory neurons. Apamin-sensitive channels may also be involved in the inhibition.
采用细胞内电生理技术记录了完整小鼠结肠体外制备物环形肌层的自发性肌电活动。在58个制备物中的34个中,周期性记录到自发性去极化(肌电复合波,MCs),约每4分钟一次。在这些制备物中,蜂毒明肽(250 nM)和N-硝基-L-精氨酸(NOLA,100 μM)分别使MCs之间的膜电位去极化8 mV或13 mV。河豚毒素(1.6 μM)消除了MCs并诱导去极化(17 mV)。在其余24个制备物中,未记录到MCs,与MCs之间的膜电位相比,膜电位显著去极化。NOLA(100 μM)、蜂毒明肽(250 nM)和河豚毒素(1.6 μM)对膜电位无显著影响。提示在表现出MC循环的制备物中,MCs之间的膜电位维持在紧张性抑制状态,主要由自发活动的抑制性神经元产生的氮能机制介导。对蜂毒明肽敏感的通道可能也参与了这种抑制作用。