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首页> 外文期刊>The European Journal of Neuroscience >Cellular and synaptic effect of substance P on neonatal phrenic motoneurons.
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Cellular and synaptic effect of substance P on neonatal phrenic motoneurons.

机译：P物质对新生儿运动神经元的细胞和突触作用。

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Experiments were carried out on the in vitro brainstem-spinal cord preparation of the newborn rat to analyse the effects of substance P (SP) on phrenic motoneuron (PMN) activity. In current-clamp mode, SP significantly depolarized PMNs, increased their input resistance, decreased the rheobase current and shifted the firing frequency-intensity relationships leftwards, but did not affect spike frequency adaptation or single spike configuration. The neurokinin receptor agonist NK1 had SP-mimetic effects, whereas the NK3 and NK2 receptor agonists were less effective and ineffective, respectively. In a tetrodotoxin-containing aCSF, only SP or the NK1 receptor agonist were still active. No depolarization was observed when the NK1 receptor agonist was applied in the presence of muscarine. In voltage-clamp mode, SP or the NK1 receptor agonist produced an inward current (ISP) which was not significantly reduced by extracellular application of tetraethylammonium, Co2+, 4-aminopyridine or Cs+. In aCSF containing tetrodotoxin, Co2+ and Cs+, ISP was blocked by muscarine. No PMN displayed any M-type potassium current but only a current showing no voltage sensitivity over the range -100 to 0 mV, reversing near the expected EK +, hence consistent with a leak current. SP application to the spinal cord only (using a partitioned chamber) significantly increased the phrenic activity. Pretreatment with the NMDA receptor antagonist DL-2-amino-5-phosphonovaleric acid (AP5) decreased the C4 discharge duration and blocked the effect of SP, thus exhibiting an NMDA potentiation by SP. In conclusion, SP modulates postsynaptically the response of phrenic motoneurons to the inspiratory drive through the reduction of a leak conductance and the potentiation of the NMDA component of the synaptic input.
机译：对新生大鼠的体外脑干-脊髓制备进行了实验，以分析物质P（SP）对运动神经元（PMN）活性的影响。在电流钳模式下，SP使PMN显着去极化，增加了它们的输入电阻，降低了流变基电流，并使点火频率-强度关系向左移动，但不影响尖峰频率适应性或单尖峰配置。神经激肽受体激动剂NK1具有SP拟态作用，而NK3和NK2受体激动剂分别无效和无效。在含有河豚毒素的aCSF中，只有SP或NK1受体激动剂仍然有效。当在毒蕈碱存在下施用NK1受体激动剂时，未观察到去极化。在电压钳模式下，SP或NK1受体激动剂产生的内向电流（ISP）不会因细胞外施加四乙铵，Co2 +，4-氨基吡啶或Cs +而显着降低。在含有河豚毒素，Co2 +和Cs +的aCSF中，ISP被毒蕈碱阻断。没有PMN显示任何M型钾电流，只有一个电流在-100至0 mV范围内没有显示电压敏感性，在期望的EK +附近反转，因此与泄漏电流一致。仅将SP应用于脊髓（使用分隔室）可显着提高the活动。用NMDA受体拮抗剂DL-2-氨基-5-膦酰戊酸（AP5）预处理可减少C4放电持续时间并阻断SP的作用，从而显示出SP对NMDA的增强作用。总之，SP通过减少漏导和突触输入的NMDA成分的增强，突触后调节of运动神经元对吸气驱动的反应。

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