Zieglgänsberger W, Tulloch I F
Brain Res. 1979 May 5;167(1):53-64. doi: 10.1016/0006-8993(79)90262-2.
Extra- and intracellular recordings were obtained from physiologically identified, spinal neurones in the 6th and 7th lumbar segments of the pentobarbitone-anaesthetized cat. Microiontophoretically applied methionine- and leucine-enkephalin reversibly inhibited the spontaneous, synaptically induced, and L-glutamate-induced activity in the majority of dorsal horn neurones studied in laminae 4, 5 and 6 of Rexed. Most of these depressant effects were antagonized by the prior microiontophoretic application of the opiate antagonist naloxone. Intracellular studies performed on dorsal horn neurones and motoneurones revealed that microiontophoretically applied methionine- and leucine-enkephalin caused no change in the resting membrane potential or the membrane resistance. Neither spike initiation nor spike overshoot were detectably altered by either enkephalin. The membrane depolarization and associated decrease in membrane resistance following microiontophoretic L-glutamate application were effectively blocked by the prior application of enkephalin. Naloxone, which by itself had no detectable effect on the membrane resistance, antagonized this effect. We propose that [enkephalinergic] cells in lamina II and III may modulate cells subserving somatosensory perception, including pain.
从戊巴比妥麻醉猫的第6和第7腰段经生理鉴定的脊髓神经元获得细胞外和细胞内记录。微量离子电泳施加的甲硫氨酸脑啡肽和亮氨酸脑啡肽可逆地抑制了在Rexed板层4、5和6中研究的大多数背角神经元的自发、突触诱导和L-谷氨酸诱导的活动。这些抑制作用大多被事先微量离子电泳施加的阿片拮抗剂纳洛酮所拮抗。对背角神经元和运动神经元进行的细胞内研究表明,微量离子电泳施加的甲硫氨酸脑啡肽和亮氨酸脑啡肽对静息膜电位或膜电阻没有影响。脑啡肽对峰电位起始和峰电位超射均无明显改变。微量离子电泳施加L-谷氨酸后出现的膜去极化和相关的膜电阻降低被事先施加的脑啡肽有效阻断。本身对膜电阻无明显影响的纳洛酮拮抗了这种作用。我们提出,板层II和III中的[脑啡肽能]细胞可能调节包括疼痛在内的躯体感觉的细胞。