Houghton A K, Clarke R W
Department of Physiology and Environmental Science, University of Nottingham, Loughborough, Leicestershire, U.K.
Neuroscience. 1995 Jun;66(3):673-83. doi: 10.1016/0306-4522(94)00608-8.
Intense natural or electrical stimulation of afferents from the toes or the heel results in prolonged changes in the excitability of the heel withdrawal reflex pathway in the rabbit. This study has investigated the roles played by tachykinin NK1 receptors in mediating these effects. Reflexes were evoked by electrical stimulation of the sural nerve and recorded from the gastrocnemius medialis muscle nerve. High-intensity electrical stimulation of the common peroneal nerve, or application of a crush stimulus to the toes, resulted in suppression of gastrocnemius reflex responses to between 30 and 50% of controls, from which recovery was complete in 15-25 min. In contrast, intense electrical stimulation of the sural nerve, or application of mustard oil to the heel, facilitated the sural to gastrocnemius reflex to two to four times control values. Recovery was rarely complete within 30 min of these stimuli. Administration of the NK1 receptor antagonist CP-96,345, but not its enantiomer CP-96,344, reduced gastrocnemius reflex responses to sural nerve stimulation per se; significantly decreased the time to recovery after common peroneal nerve stimulation and toe crush (but did not affect maximum inhibition); and significantly reduced the facilitation of reflexes resulting from sural nerve stimulation or mustard oil applied to the heel in the first 3-5 min after the application of the stimuli. Both CP-96,345 and CP-96,344 reduced blood pressure and heart rate. These data show that: (i) blockade of NK1-receptors reduces excitatory drive from sural nerve afferents to GM motoneurones; (ii) NK1-receptors are involved in the generation of the early excitatory events which follow stimulation of nociceptive afferents from the heel; and (iii) have a role in the later stages of prolonged, opioid-mediated inhibition of reflexes resulting from activation of fine afferents from the toes. We believe that (ii) and (iii) reflect a role for tachykinins as transmitters from small diameter primary afferent fibres.
对兔的脚趾或足跟传入神经进行强烈的自然刺激或电刺激，会导致足跟退缩反射通路的兴奋性发生长时间变化。本研究调查了速激肽NK1受体在介导这些效应中所起的作用。通过电刺激腓肠神经诱发反射，并从腓肠内侧肌神经记录。对腓总神经进行高强度电刺激，或对脚趾施加挤压刺激，会导致腓肠肌反射反应抑制至对照值的30%至50%，15 - 25分钟后完全恢复。相比之下，对腓肠神经进行强烈电刺激，或在足跟涂抹芥子油，会使腓肠神经到腓肠肌的反射增强至对照值的两到四倍。这些刺激后30分钟内很少完全恢复。给予NK1受体拮抗剂CP - 96,345，但不给予其对映体CP - 96,344，可降低腓肠肌对腓肠神经刺激本身的反射反应；显著缩短腓总神经刺激和脚趾挤压后恢复的时间（但不影响最大抑制程度）；并显著降低刺激后最初3 - 5分钟内腓肠神经刺激或足跟涂抹芥子油所导致的反射增强。CP - 96,345和CP - 96,344均降低血压和心率。这些数据表明：（i）阻断NK1受体会减少腓肠神经传入纤维对腓肠肌运动神经元的兴奋性驱动；（ii）NK1受体参与了足跟伤害性传入纤维刺激后早期兴奋性事件的产生；（iii）在由脚趾细传入纤维激活导致的阿片类药物介导的反射长时间抑制的后期阶段起作用。我们认为（ii）和（iii）反映了速激肽作为小直径初级传入纤维递质的作用。
