对侧腹外侧索电刺激在离体脊髓运动神经元诱发突触反应的特性

目的:了解对侧腹外侧索(cVLF)至离体脊髓运动神经元(MN)突触传递的细胞电生理特性和介导递质。方法:应用新生大鼠(8～14d)脊髓切片MN细胞内记录技术,观察电刺激cVLF在MN所诱发的突触反应及其药理学特性。结果:在49个测试的MN上,观察到cVLF电刺激可在25个MN上诱发去极化反应(即cVLF兴奋性突触后电位,cVLF-EPSP),在2个MN上诱发超极化反应(即cVLF抑制性突触后电位,cVLF-IPSP),在3个MN上诱发cVLF-EP-SP复合cVLF-IPSP的反应。cVLF-EPSP具有刺激强度依赖性、膜电位依赖性、被TTX可逆性取消和双脉冲易化的特性。NMDA受体阻断剂APV(30μmol/L)、非NMDA受体阻断剂DNQX(1μmol/L)均可抑制cVLF-EPSP,并显现出cV-LF-IPSP成分,该成分主要对甘氨酸受体阻断剂士的宁敏感。结论:cVLF电刺激可在MN诱导谷氨酸能的cVLF-EPSP和甘氨酸能为主的cVLF-IPSP,介导对侧下行激活通路对MN功能的调制。

Characteristics of synaptic responses evoked by electrical stimulation of contralateral ventrolateral funiculus in spinal cord motoneurons in vitro

Objective：To explore the characteristics of the synaptic transmission from contralateral ventrolateral funieulus （eVLF） to motoneurons （MNs） in neonatal rat spinal cord slices. Methods： The intraeellular reeordings were performed in MN of spinal cord slices isolated from neonatal rats （8 -14 days old） ,and cVLF stimulation was applied to activate the descending fibers. Some selective excitatory or inhibitory amino acid receptor antagonists were also used to identify the responsible transmitters. Results： Among 49 tested MNs, depolarizing responses （excitatory. postsynaptie potentials, EPSPs） were elicited by cVLF stimulation （cVLF-EPSPs） in 25 MNs, hyperpolarizing responses （ inhibitory postsynaptic potential,IPSPs,i, e. cVLF-IPSPs） in 2 MNs,and cVLF-IPSPs preceded by cVLF-EPSPs in 3 MNs. The eVLF-EPSPs were characterized by stimulus intensity-dependent, membrane potential-dependent, tetrodotoxinsensitive and paired-pulse facilitative properties. Both of NMDA receptor antagonist APV （30 μmol/L） and non-NMDA receptor antagonist DNQX （ 1 μmol/L） could reduce cVLF-EPSP and showed a cVLF-IPSP component, which was nullified by glycine receptor antagonist strychnine （1 μmol/L）. Conclusion： These results suggest that the synaptic responses evoked by cVLF stimulation in MNs may include glutamate receptor-mediated cVLF-EPSP and glyclne receptor-mediated cVLF-IPSP to conduct modulation of MNs by contralateral descending activation.