Neural Engineering Laboratory, Department of Biomedical Engineering, The City College of the City University of New York, City College Center for Discovery and Innovation, New York, NY 10031
Neural Engineering Laboratory, Department of Biomedical Engineering, The City College of the City University of New York, City College Center for Discovery and Innovation, New York, NY 10031.
eNeuro. 2023 May 17;10(5). doi: 10.1523/ENEURO.0429-22.2023. Print 2023 May.
Spinal cord stimulation (SCS) evokes fast epidural evoked compound action potential (ECAP) that represent activity of dorsal column axons, but not necessarily a spinal circuit response. Using a multimodal approach, we identified and characterized a delayed and slower potential evoked by SCS that reflects synaptic activity within the spinal cord. Anesthetized female Sprague Dawley rats were implanted with an epidural SCS lead, epidural motor cortex stimulation electrodes, an epidural spinal cord recording lead, an intraspinal penetrating recording electrode array, and intramuscular electromyography (EMG) electrodes in the hindlimb and trunk. We stimulated the motor cortex or the epidural spinal cord and recorded epidural, intraspinal, and EMG responses. SCS pulses produced characteristic propagating ECAPs (composed of P1, N1, and P2 waves with latencies <2 ms) and an additional wave ("S1") starting after the N2. We verified the S1-wave was not a stimulation artifact and was not a reflection of hindlimb/trunk EMG. The S1-wave has a distinct stimulation-intensity dose response and spatial profile compared with ECAPs. 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX; a selective competitive antagonist of AMPA receptors (AMPARs)] significantly diminished the S1-wave, but not ECAPs. Furthermore, cortical stimulation, which did not evoke ECAPs, produced epidurally detectable and CNQX-sensitive responses at the same spinal sites, confirming epidural recording of an evoked synaptic response. Finally, applying 50-Hz SCS resulted in dampening of S1-wave but not ECAPs. Therefore, we hypothesize that the S1-wave is synaptic in origin, and we term the S1-wave type responses: evoked synaptic activity potentials (ESAPs). The identification and characterization of epidurally recorded ESAPs from the dorsal horn may elucidate SCS mechanisms.
脊髓刺激 (SCS) 会引发快速硬膜外诱发复合动作电位 (ECAP),代表背柱轴突的活动,但不一定是脊髓回路的反应。我们采用多模态方法,鉴定并描述了一种由 SCS 诱发的延迟且较慢的电位,该电位反映了脊髓内的突触活动。将雌性 Sprague Dawley 大鼠麻醉并植入硬膜外 SCS 引线、硬膜外运动皮层刺激电极、硬膜外脊髓记录引线、脊髓内穿透记录电极阵列和后肢和躯干的肌内肌电图 (EMG) 电极。我们刺激运动皮层或硬膜外脊髓,并记录硬膜外、脊髓内和 EMG 反应。SCS 脉冲产生特征性传播的 ECAP(由潜伏期 <2 ms 的 P1、N1 和 P2 波组成)和 N2 后开始的附加波(“S1”)。我们验证了 S1 波不是刺激伪影,也不是后肢/躯干 EMG 的反射。与 ECAP 相比,S1 波具有独特的刺激强度剂量反应和空间分布。6-氰基-7-硝基喹喔啉-2,3-二酮 (CNQX;AMPA 受体 (AMPAR) 的选择性竞争性拮抗剂)显著减弱了 S1 波,但不减弱 ECAP。此外,皮质刺激不会引发 ECAP,但会在相同的脊髓部位产生可检测到的硬膜外和 CNQX 敏感反应,证实了诱发突触反应的硬膜外记录。最后,施加 50-Hz SCS 导致 S1 波减弱,但不减弱 ECAP。因此,我们假设 S1 波是突触起源的,我们将 S1 波类型的反应命名为:诱发的突触活动电位 (ESAP)。从背角硬膜外记录 ESAP 的鉴定和描述可能阐明 SCS 机制。