Differential modulation of disynaptic cutaneous inhibition and excitation in ankle flexor motoneurons during fictive locomotion
Differential modulation of disynaptic cutaneous inhibition and excitation in ankle flexor motoneurons during fictive locomotion
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DOI：
10.1152/jn.1996.76.5.2972
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发表时间：
1996-11-01
影响因子：
2.5
通讯作者：
Burke, RE
中科院分区：
文献类型：
--
作者：
Degtyarenko, MA;Simon, ES;Burke, RE
1. 在虚构运动过程中，使用趾长伸肌 (EDL) 和胫骨前肌 (TA) α 运动神经元的细胞内记录来检查未麻醉、去大脑成年猫对腓浅皮肤 (SP) 和足底内侧 (MPL) 神经进行电刺激产生的寡突触后电位 (PSP) 的调制模式。2.在研究的所有 20 个 EDL 运动神经元中，在休息时和虚构步进的延伸阶段，用单脉冲对神经中最易兴奋的纤维 (2xT) 进行约两倍阈值的单脉冲电刺激，要么不产生突触电位，要么产生相对较小的寡突触兴奋性或抑制性 PSP（EPSP 或 IPSP）。然而，在屈曲阶段开始时，SP 响应中出现了大的、可能是非突触的 IPSP（中心延迟 1.7-2.0 ms）。尽管保持膜去极化，这些 IPSP 通常在屈曲期后期振幅下降。3．在大多数 (7/8) TA 运动神经元中，SP 刺激在休息时和虚拟步进的延伸阶段产生寡突触 EPSP。在所研究的大多数 TA 细胞 (5/8) 中，这些 EPSP 在屈曲期间受到抑制，但在任何 TA 运动神经元中均未发现明显的突触性 IPSP。4。在大多数 EDL 和 TA 运动神经元中，MPL 神经的刺激在休息和伸展阶段产生寡突触 EPSP，大多数的潜伏期在可能的非突触范围内（小于或等于 2.0 ms）。当存在时，在几乎所有检查的 EDL (18/20) 和 TA (6/5) 运动神经元中，这些 MPL EPSP 在整个迈步屈曲阶段都受到抑制。5。现有证据表明，虚构步进过程中的这些调节效应主要是由于来自脊髓中枢模式发生器（CPG）的控制信息的收敛，用于运动到寡突触皮肤通路中的节段中间神经元上。6。这些观察结果为运动 CPG 通过猫后肢皮肤反射通路精确差异控制传播提供了证据。结合有关指长屈肌 (FDL) 运动神经元中皮肤 PSP 运动调节的早期证据，数据表明，部分由 SP 神经携带的足背表面的皮肤信息，通过离散的末阶中间神经元组投射到指运动神经元（FDL 和 EDL），这些中间神经元在屈曲期间也接收来自运动 CPG 的强大激发。相反，将兴奋信息从 SP 神经传递到至少一些 TA 运动神经元的末阶中间神经元在屈曲过程中受到 CPG 的抑制。7．另一个对比在于，在运动的屈曲阶段，FDL、EDL 和 TA 运动神经元通过 MPL 神经从足底表面发出的寡突触皮肤兴奋受到抑制。现有的信息与 MPL 效应可能通过常见的中间神经元传递到这些运动核的可能性是一致的。8。我们提出了一种中间神经元电路，可以解释这些观察结果，并讨论运动过程中这些感觉通路调节的可能功能影响。
1. Intracellular recording from extensor digitorum longus (EDL) and tibialis anterior (TA) alpha-motoneurons during fictive locomotion was used to examine patterns of modulation of oligo synaptic postsynaptic potentials (PSPs) produced by electrical stimulation of the cutaneous superficial peroneal (SP) and medial plantar (MPL) nerves in unanesthetized, decerebrate adult cats.2. In all 20 EDL motoneurons studied, electrical stimulation of the SP nerve with single pulses at about twice threshold for the most excitable fibers in the nerve (2xT) produced either no synaptic potentials or relatively small oligosynaptic excitatory or Inhibitory PSPs (EPSPs or IPSPs), both at rest and during the extension phase of Fictive stepping. However, at the onset of the flexion phase large, presumably disynaptic IPSPs (central latencies 1.7-2.0 ms) appeared in the SP responses. These IPSPs usually decreased in amplitude later in the flexion phase despite maintained membrane depolarization.3. In most (7/8) TA motoneurons, SP stimulation produced oligosynaptic EPSPs at rest and during the extension phase of fictive stepping. These EPSPs were suppressed during flexion in a majority of TA cells studied (5/8) but no clearly disynaptic IPSPs were found in any TA motoneuron.4. In most EDL and TA motoneurons, stimulation of the MPL nerve produced oligosynaptic EPSPs at rest and during the extension phase, most with latencies in the presumably disynaptic range (less than or equal to 2.0 ms). When present, these MPL EPSPs were suppressed throughout the flexion phase of stepping in almost all EDL (18/20) and TA (6/5) motoneurons examined.5. The available evidence suggests that these modulation effects during fictive stepping are due primarily to convergence of control information from the spinal central pattern generator (CPG) for locomotion onto segmental interneurons in the oligosynaptic cutaneous pathways.6. These observations extend the evidence for precise differential control of transmission through cutaneous reflex pathways in the cat hindlimb by the locomotor CPG. Taken together with earlier evidence about locomotor modulation of cutaneous PSPs in flexor digitorum longus (FDL) motoneurons, the data suggest that cutaneous information from the dorsal surface of the foot, carried in part by the SP nerve, projects to digit motoneurons (FDL and EDL) through discrete sets of last-order interneurons that also receive powerful excitation from the locomotor CPG during flexion. In contrast, the last-order interneurons that convey excitatory information from the SP nerve to at least some TA motoneurons are inhibited by the CPG during flexion.7. Another contrast resides in the fact that oligosynaptic cutaneous excitation from the plantar surface of the foot, via the MPL nerve, is suppressed in FDL, EDL, and TA motoneurons during the flexion phase of locomotion. The available Information is consistent with the possibility that MPL effects may be delivered to these motor nuclei by common interneurons.8. We suggest an interneuronal circuitry that could account for these observations and discuss possible functional implications of modulation of these sensory pathways during locomotion.