De Koninck Y, Henry J L
Department of Physiology, McGill University, Montréal, Quebec, Canada.
Neuroscience. 1992 Sep;50(2):435-43. doi: 10.1016/0306-4522(92)90435-5.
We have previously reported a vibration-induced, adenosine-mediated inhibition of nociceptive dorsal horn neurons in the cat spinal cord. The present study was conducted to investigate the mechanisms of this inhibition. In vivo intracellular recording was obtained from dorsal horn neurons in the lower lumbar segments of the anaesthetized cat. Vibration (80-250 Hz for 2-3 s every 15-20 s) was applied to the glabrous skin of the toes of the hind foot using a feedback-controlled mechanical stimulator. In 32 of 43 neurons tested, vibration produced a pronounced hyperpolarization of the membrane potential. This hyperpolarization peaked at -10 mV and decayed throughout the period of the application of vibration. It was associated with a decrease in membrane resistance, had a reversal potential negative to the resting membrane potential and was Cl(-)-independent, suggesting that it was due to an increase in a K+ conductance, properties typical of the response to adenosine. This inhibitory postsynaptic potential was unaffected by intravenous administration of bicuculline, strychnine and naloxone but was blocked by iontophoretic administration of 8-sulphophenyltheophylline, a P1-purinergic receptor antagonist. These results confirm our previous finding that vibration-induced inhibition of nociceptive dorsal horn neurons is mediated via the release of an endogenous purine compound and further suggests that this inhibition involves a postsynaptic inhibitory mechanism.
我们之前报道过,振动诱导的、腺苷介导的对猫脊髓中伤害性背角神经元的抑制作用。本研究旨在探究这种抑制作用的机制。通过在麻醉猫的下腰段背角神经元进行体内细胞内记录。使用反馈控制的机械刺激器,对后足趾无毛皮肤施加振动(每15 - 20秒施加80 - 250 Hz的振动2 - 3秒)。在测试的43个神经元中的32个中,振动使膜电位产生明显的超极化。这种超极化在 - 10 mV时达到峰值,并在振动施加期间逐渐衰减。它与膜电阻降低相关,其反转电位比静息膜电位更负,且与Cl(-)无关,这表明它是由于K+电导增加所致,这是对腺苷反应的典型特性。这种抑制性突触后电位不受静脉注射荷包牡丹碱、士的宁和纳洛酮的影响,但被离子电泳施加的P1 - 嘌呤能受体拮抗剂8 - 磺基苯基茶碱所阻断。这些结果证实了我们之前的发现,即振动诱导的对伤害性背角神经元的抑制是通过内源性嘌呤化合物的释放介导的,并且进一步表明这种抑制涉及一种突触后抑制机制。