Roberts A, Dale N, Evoy W H, Soffe S R
J Neurophysiol. 1985 Jul;54(1):1-10. doi: 10.1152/jn.1985.54.1.1.
Embryos spinalized at the 3rd to 6th postotic myotome and immobilized in 10(-4) M tubocurarine can respond to a brief skin stimulus with motor root activity suitable for swimming. Embryos spinalized at the more caudal levels give shorter episodes of fictive swimming. We have previously described the synaptic inputs to motoneurons during fictive swimming in intact embryos (23). In the present paper we look to see if similar synaptic inputs are present in spinal embryos and are therefore spinal in origin. All motoneuron firing during fictive swimming is associated with a tonic depolarization that falls away slowly once firing stops, is increased by hyperpolarizing current, and is reduced by depolarizing current. A slow depolarizing potential evoked by lower levels of skin stimulation has similar properties and rate of fall. In 1-2 mM PDA, an excitatory amino acid antagonist, only a small remnant of the depolarization remains, and motoneuron firing stops. The NMDA antagonist 50 microM APV reduces the depolarization less but also blocks firing. Motoneurons fire one spike per swimming cycle, in phase with nearby motor root discharge. Spikes are preceded by a depolarizing prepotential. This increases with hyperpolarizing current, which can block the spike to reveal an underlying depolarizing potential. In phase with motor root discharge on the opposite side of the body, motoneurons receive a midcycle inhibitory postsynaptic potential, which increases with depolarizing current, decreases with hyperpolarizing current, and is blocked by 10(-6) M strychnine. Strychnine, 5 X 10(-7) M, leads first to broadening of motor root bursts then to loss of the alternating swimming pattern of activity, which is replaced by synchronous bursts on both sides of the body. We conclude that the synaptic inputs to motoneurons during fictive swimming in spinal embryos are very similar in properties and pharmacology to those in intact embryos. These inputs, including the tonic depolarization always associated with motoneuron firing during swimming, must be at least partly spinal in origin.
在第3至6个耳后肌节处脊髓横断并固定于10⁻⁴ M筒箭毒碱中的胚胎,能对短暂的皮肤刺激产生适合游泳的运动根活动反应。在更靠尾端水平脊髓横断的胚胎,其虚构游泳发作时间较短。我们之前已经描述了完整胚胎在虚构游泳期间运动神经元的突触输入(23)。在本文中,我们探究脊髓胚胎中是否存在类似的突触输入,以及这些输入是否源于脊髓。虚构游泳期间所有运动神经元的放电都与一个强直去极化相关,一旦放电停止,该去极化会缓慢消退,通过超极化电流可增强,通过去极化电流可减弱。较低水平皮肤刺激诱发的缓慢去极化电位具有相似的特性和下降速率。在1 - 2 mM的兴奋性氨基酸拮抗剂PDA中,仅残留少量去极化,运动神经元放电停止。50 μM的NMDA拮抗剂APV对去极化的降低作用较小,但也会阻断放电。运动神经元在每个游泳周期发放一个动作电位,与附近的运动根放电同步。动作电位之前有一个去极化预电位。它随着超极化电流增加,超极化电流可阻断动作电位以揭示潜在的去极化电位。与身体另一侧的运动根放电同步,运动神经元在周期中期接受抑制性突触后电位,该电位随着去极化电流增加,随着超极化电流减小,并被10⁻⁶ M士的宁阻断。5×10⁻⁷ M的士的宁首先导致运动根爆发增宽,然后导致交替的游泳活动模式丧失,取而代之的是身体两侧的同步爆发。我们得出结论,脊髓胚胎在虚构游泳期间运动神经元的突触输入在特性和药理学上与完整胚胎中的非常相似。这些输入,包括游泳期间总是与运动神经元放电相关的强直去极化,其起源至少部分是脊髓性的。