Glutamatergic N2v cells are central pattern generator interneurons of the Lymnaea feeding system:: New model for rhythm generation
Glutamatergic N2v cells are central pattern generator interneurons of the Lymnaea feeding system:: New model for rhythm generation
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谷氨酸能N2v细胞是蛙类摄食系统的中心模式发生中间神经元：..： 节律产生的新模型
DOI：
10.1152/jn.1997.78.6.3396
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发表时间：
1997-12-01
影响因子：
2.5
通讯作者：
Benjamin, PR
中科院分区：
文献类型：
--
作者：
Brierley, MJ;Yeoman, MS;Benjamin, PR
我们的目的是表明，成对的N2 v（N2腹侧）的颊神经节的平台细胞是重要的中央模式发生器（CPG）的神经元的神经元的摄食系统。N2 v平台化在慢振荡器（SO）驱动的虚构馈送节律中锁相到CPG网络的其余部分。节律的相位由人工诱发的N2 v爆发重置，这是CPG神经元的特征。N2 v细胞与CPG网络的其余部分以及调节性SO细胞和脑巨细胞（CGC）具有广泛的输入和输出突触连接。来自延长期中间神经元N1 M（兴奋性）、NIL（抑制性）和SO（兴奋性-兴奋性）的突触输入可能有助于触发N2 v平台的斜坡形前电位。前电位具有高度复杂的波形，这是由于组成突触电位的幅度的渐进变化。最重要的是促进SO -> N2 v单突触连接的兴奋成分。其他CPG中间神经元都没有合适的输入突触连接来终止N2 v平台。研究了SO和N1 M/N1 Ls的递质乙酰胆碱（ACh）的调节功能。将ACh（50 ms脉冲）局部应用于N2 v细胞，再现了SO --> N2 v双相突触反应，但也诱导了长期平台期（20-60 s）。N2 d细胞没有表现出内源性的高原能力，但这可以通过ACh的局部应用来诱导。N2 v细胞抑制N3紧张性（N3 t），但不抑制N3相性（N3 p）CPG中间神经元。N2 v-->t N3 t抑制性突触连接在定时N3 t活性中是重要的。N3 t细胞从这种抑制中恢复，并在进食模式的吞咽阶段期间放电。反馈N2 v抑制SO，N1 L延长相中间神经元，防止他们在收缩期的喂养周期。N2 v--> N1 M突触连接较弱，仅在50%的制备物中发现。弱N2 v--> CGC抑制连接阻止CGC在进食周期的锉（N2）阶段期间放电。这些数据允许一个新的模式，拟提出的食CPG的。这强调了六种类型的CPG中间神经元中的每一种都有一组独特的突触连接，所有这些都有助于产生完整的CPG模式。
We aimed to show that the paired N2v (N2 ventral) plateauing cells of the buccal ganglia are important central pattern generator (CPG) interneurons of the Lymnaea feeding system. N2v plateauing is phase-locked to the rest of the CPG network in a slow oscillator (SO)-driven fictive feeding rhythm. The phase of the rhythm is reset by artificially evoked N2v bursts, a characteristic of CPG neurons. N2v cells have extensive input and output synaptic connections with the rest of the CPG network and the modulatory SO cell and cerebral giant cells (CGCs). Synaptic input from the protraction phase interneurons N1M (excitatory), NIL(inhibitory), and SO (inhibitory-excitatory) are likely to contribute to a ramp-shaped prepotential that triggers the N2v plateau. The prepotential has a highly complex waveform due to progressive changes in the amplitude of the component synaptic potentials. Most significant is the facilitation of the excitatory component of the SO --> N2v monosynaptic connection. None of the other CPG interneurons has the appropriate input synaptic connections to terminate the N2v plateaus. The modulatory function of acetylcholine (ACh), the transmitter of the SO and N1M/N1Ls, was examined. Focal application of ACh (50-ms pulses) onto the N2v cells reproduced the SO --> N2v biphasic synaptic response but also induced long-term plateauing (20-60 s). N2d cells show no endogenous ability to plateau, but this can be induced by focal applications of ACh. The N2v cells inhibit the N3 tonic (N3t) but not the N3 phasic (N3p) CPG interneurons. The N2v -->t N3t inhibitory synaptic connection is important in timing N3t activity. The N3t cells recover from this inhibition and fire during the swallow phase of the feeding pattern. Feedback N2v inhibition to the SO, N1L protraction phase interneurons prevents them firing during the retraction phase of the feeding cycle. The N2v --> N1M synaptic connection was weak and only found in 50% of preparations. A weak N2v --> CGC inhibitory connection prevents the CGCs firing during the rasp (N2) phase of the feeding cycle. These data allowed a new model for the Lymnaea feeding CPG to be proposed. This emphasizes that each of the six types of CPG interneuron has a unique set of synaptic connections, all of which contribute to the generation of a full CPG pattern.