Zhang K M, Wang X M, Peterson A M, Chen W Y, Mokha S S
Department of Anatomy and Physiology, Meharry Medical College, Nashville, Tennessee 37208, USA.
J Neurophysiol. 1998 Oct;80(4):2210-4. doi: 10.1152/jn.1998.80.4.2210.
Extracellular single unit recordings were made from neurons in the superficial and deeper dorsal horn of the medulla (trigeminal nucleus caudalis) in 21 male rats anesthetized with urethan. NMDA produced an antagonist-reversible excitation of 46 nociceptive as well as nonnociceptive neurons. Microiontophoretic application of a preferential alpha2-adrenoceptor (alpha2AR) agonist, (2-[2, 6-dichloroaniline]-2-imidazoline) hydrochloride (clonidine), reduced the NMDA-evoked responses of 86% (6/7) of nociceptive-specific (NS) neurons, 82% (9/11) of wide dynamic range (WDR) neurons, and 67% (4/6) of low-threshold (LT) neurons in the superficial dorsal horn. In the deeper dorsal horn, clonidine inhibited the NMDA-evoked responses of 94% (16/17) of NS and WDR neurons and 60% (3/5) of LT neurons. Clonidine facilitated the NMDA-evoked responses in 14% (1/17) of NS, 9% (1/11) of WDR, and 33% (2/6) of LT neurons in the superficial dorsal horn. Idazoxan, an alpha2AR antagonist, reversed the inhibitory effect of clonidine in 90% (9/10) of neurons, whereas prazosin, an alpha1-adrenoceptor antagonist with affinity for alpha2BAR, and alpha2CAR, were ineffective. We suggest that activation of alpha2ARs produces a predominantly inhibitory modulation of the NMDA-evoked responses of nociceptive neurons in the medullary dorsal horn.
在21只经乌拉坦麻醉的雄性大鼠中，从延髓（三叉神经尾侧核）浅层和深层背角的神经元进行细胞外单单位记录。N-甲基-D-天冬氨酸（NMDA）对46个伤害性和非伤害性神经元产生了拮抗剂可逆性兴奋。微量离子电泳应用优先的α2-肾上腺素能受体（α2AR）激动剂盐酸（2-[2,6-二氯苯胺]-2-咪唑啉）（可乐定），减少了浅层背角中86%（6/7）的伤害性特异性（NS）神经元、82%（9/11）的广动力范围（WDR）神经元和67%（4/6）的低阈值（LT）神经元的NMDA诱发反应。在深层背角，可乐定抑制了94%（16/17）的NS和WDR神经元以及60%（3/5）的LT神经元的NMDA诱发反应。可乐定使浅层背角中14%（1/17）的NS、9%（1/11）的WDR和33%（2/6）的LT神经元的NMDA诱发反应增强。α2AR拮抗剂咪唑克生在90%（9/10）的神经元中逆转了可乐定的抑制作用，而对α2BAR和α2CAR有亲和力的α1-肾上腺素能受体拮抗剂哌唑嗪则无效。我们认为，α2AR的激活对延髓背角伤害性神经元的NMDA诱发反应产生主要的抑制性调节。
