Department of Physiology, School of Biomedical Sciences, University of Melbourne, Parkville, Australia.
PLoS Comput Biol. 2022 Jun 13;18(6):e1009717. doi: 10.1371/journal.pcbi.1009717. eCollection 2022 Jun.
Transmission between neurons in the extensive enteric neural networks of the gut involves synaptic potentials with vastly different time courses and underlying conductances. Most enteric neurons exhibit fast excitatory post-synaptic potentials (EPSPs) lasting 20-50 ms, but many also exhibit slow EPSPs that last up to 100 s. When large enough, slow EPSPs excite action potentials at the start of the slow depolarization, but how they affect action potentials evoked by fast EPSPs is unknown. Furthermore, two other sources of synaptic depolarization probably occur in enteric circuits, activated via GABAA or GABAC receptors; how these interact with other synaptic depolarizations is also unclear. We built a compartmental model of enteric neurons incorporating realistic voltage-dependent ion channels, then simulated fast EPSPs, slow EPSPs and GABAA or GABAC ligand-gated Cl- channels to explore these interactions. Model predictions were tested by imaging Ca2+ transients in myenteric neurons ex vivo as an indicator of their activity during synaptic interactions. The model could mimic firing of myenteric neurons in mouse colon evoked by depolarizing current during intracellular recording and the fast and slow EPSPs in these neurons. Subthreshold fast EPSPs evoked spikes during the rising phase of a slow EPSP, but suprathreshold fast EPSPs could not evoke spikes later in a slow EPSP. This predicted inhibition was confirmed by Ca2+ imaging in which stimuli that evoke slow EPSPs suppressed activity evoked by fast EPSPs in many myenteric neurons. The model also predicted that synchronous activation of GABAA receptors and fast EPSPs potentiated firing evoked by the latter, while synchronous activation of GABAC receptors with fast EPSPs, potentiated firing and then suppressed it. The results reveal that so-called slow EPSPs have a biphasic effect being likely to suppress fast EPSP evoked firing over very long periods, perhaps accounting for prolonged quiescent periods seen in enteric motor patterns.
肠道广泛的肠神经网络中的神经元之间的传递涉及具有非常不同时间进程和潜在电导的突触电位。大多数肠神经元表现出持续 20-50 毫秒的快速兴奋性突触后电位 (EPSP),但许多神经元也表现出持续长达 100 秒的慢速 EPSP。当足够大时,慢速 EPSP 在慢速去极化开始时激发动作电位,但它们如何影响由快速 EPSP 激发的动作电位尚不清楚。此外,肠回路中可能还存在另外两种源自突触去极化的来源,通过 GABAA 或 GABAC 受体激活;这些如何与其他突触去极化相互作用尚不清楚。我们构建了一个包含现实电压依赖性离子通道的肠神经元分区模型,然后模拟了快速 EPSP、慢速 EPSP 以及 GABAA 或 GABAC 配体门控 Cl-通道,以探索这些相互作用。通过在体外用钙成像记录来测试模型预测,作为突触相互作用期间神经元活动的指标。该模型可以模拟在体内记录期间用去极化电流激发的小鼠结肠肌间神经元的放电以及这些神经元中的快速和慢速 EPSP。亚阈值快速 EPSP 在慢速 EPSP 的上升相期间引发尖峰,但超阈值快速 EPSP 不能在慢速 EPSP 的后期引发尖峰。钙成像证实了这种预测的抑制作用,在这种成像中,诱发慢速 EPSP 的刺激抑制了许多肌间神经元中由快速 EPSP 诱发的活动。该模型还预测,GABAA 受体和快速 EPSP 的同步激活增强了后者引发的放电,而 GABAC 受体与快速 EPSP 的同步激活增强了放电,然后抑制了放电。结果表明,所谓的慢速 EPSP 具有双相作用,可能在很长一段时间内抑制由快速 EPSP 诱发的放电,这也许可以解释在肠运动模式中观察到的长时间静止期。