Rioult-Pedotti M S
Department of Biology, Yale University, New Haven, Connecticut 06520-8103, USA.
J Neurophysiol. 1997 Feb;77(2):717-30. doi: 10.1152/jn.1997.77.2.717.
Low-frequency membrane potential oscillations were induced in motoneurons (MNs) of isolated hemisected frog spinal cords during N-methyl-D-aspartate (NMDA) application. Oscillations required the presence of physiological Mg2+ and preincubation with strychnine, whereas incubation with bicuculline or phaclofen was not effective. Oscillations were evident in intracellular recordings from single MNs and simultaneous extracellular recordings from lumbar ventral roots. In Mg(2+)-free solution, MNs exhibited irregular transient membrane potential depolarizations that were blocked by D,L-2-amino-5-phosphonopentanoic acid (APV) but not by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Generation and maintenance of membrane potential oscillations required specific NMDA receptor activation. Oscillations were antagonized by APV but not by CNQX. Strychnine preincubation was required for NMDA to induce oscillations, but was not critical in maintaining them, because oscillations persisted after removal of strychnine. Therefore oscillations are suggested to be an inherent property of the spinal neuronal circuitry. Tetrodotoxin (TTX) blocked spike activity and had a bimodal effect on membrane potential oscillations. Oscillations initially were blocked by TTX, but reappeared spontaneously after 10-40 min. This suggests that maintenance of oscillations, once evoked, does not involve MN firing. Na+ entry through TTX-insensitive Na+ channels and/or NMDA receptor channels, trans-membrane Ca2+ flux, Ca2+ release from intracellular stores, and Ca2+ activated K+ channels were critical in controlling the amplitude and frequency of membrane potential oscillations. It is hypothesized that these unmasked intrinsic oscillations in adult frog spinal cord MNs may represent a premetamorphic spinal oscillator involved in tadpole swimming that becomes suppressed during metamorphosis as strychnine-sensitive inhibition becomes more pronounced.
在应用N-甲基-D-天冬氨酸（NMDA）期间，在分离的半切青蛙脊髓的运动神经元（MNs）中诱发了低频膜电位振荡。振荡需要生理浓度的Mg2+存在以及与士的宁预孵育，而与荷包牡丹碱或巴氯芬孵育则无效。在单个MN的细胞内记录以及腰腹根的同步细胞外记录中，振荡很明显。在无Mg(2+)的溶液中，MN表现出不规则的瞬时膜电位去极化，这些去极化被D,L-2-氨基-5-膦酰戊酸（APV）阻断，但不被6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）阻断。膜电位振荡的产生和维持需要特定的NMDA受体激活。振荡被APV拮抗，但不被CNQX拮抗。士的宁预孵育是NMDA诱导振荡所必需的，但对维持振荡并不关键，因为去除士的宁后振荡仍持续存在。因此，振荡被认为是脊髓神经元回路的固有特性。河豚毒素（TTX）阻断了动作电位活动，并对膜电位振荡有双峰效应。振荡最初被TTX阻断，但在10 - 40分钟后自发重新出现。这表明一旦诱发，振荡的维持不涉及MN放电。通过TTX不敏感的Na+通道和/或NMDA受体通道的Na+内流、跨膜Ca2+通量、细胞内储存的Ca2+释放以及Ca2+激活的K+通道在控制膜电位振荡的幅度和频率方面至关重要。据推测，成年青蛙脊髓MNs中这些未被掩盖的固有振荡可能代表一种参与蝌蚪游泳的变态前脊髓振荡器，在变态过程中随着士的宁敏感抑制变得更加明显而被抑制。
