Light A R, Willcockson H H
Department of Cell and Molecular Physiology and Curriculum in Neurobiology, University of North Carolina, Chapel Hill, North Carolina 27599-7545, USA.
J Neurophysiol. 1999 Dec;82(6):3316-26. doi: 10.1152/jn.1999.82.6.3316.
Using the in vivo whole cell recording procedure described previously, we recorded 73 neurons in laminae I and II in the lumbar spinal cord of the rat. Input impedances averaged 332 MOmega, which indicated that prior sharp electrode recordings contained a significant current shunt. Characterization of the adequate stimuli from the excitatory hindlimb receptive field indicated that 39 of 73 neurons were nociceptive, 6 were innocuous cooling cells, 20 responded maximally to brush, and 8 cells were not excited by stimulation of the skin of the hindlimb. The locations of 15 neurons were marked with biocytin. Nociceptive neurons were mostly found in lamina I and outer II, cooling cells in lamina I, and innocuous mechanoreceptive cells were mostly found in inner II or in the overlying white matter. The mu-opioid agonist [D-Ala(2), N-Me-Phe(4), Gly(5)-ol]-Enkephalin (DAMGO) hyperpolarized 7 of 19 tested neurons with a conductance increase. This hyperpolarization was reversed by naloxone in the neurons in which it was applied. DAMGO also decreased the frequency of spontaneous PSPs in 13 neurons, 7 of which were also hyperpolarized by DAMGO. Five of the seven hyperpolarized neurons were nociceptive, responding to both heat and mechanically noxious stimuli, whereas two responded to slow, innocuous brush. These results indicate that whole cell, tight seal recordings sample a similar population of lamina I and II neurons in the rat as those found with sharp electrode recordings in cat and monkey. They further indicate that DAMGO hyperpolarizes a subset of the nociceptive neurons that have input from both heat and mechanical nociceptors and that presynaptic DAMGO effects can be observed in nociceptive neurons that are not hyperpolarized by DAMGO.
采用先前描述的体内全细胞记录程序，我们在大鼠腰脊髓的I层和II层记录了73个神经元。输入阻抗平均为332兆欧，这表明先前的尖锐电极记录存在明显的电流分流。对来自兴奋性后肢感受野的适宜刺激进行特性分析表明，73个神经元中有39个是伤害性感受神经元，6个是无害冷觉细胞，20个对轻刷刺激反应最大，8个细胞对后肢皮肤刺激无兴奋反应。用生物胞素标记了15个神经元的位置。伤害性感受神经元大多位于I层和II层外侧，冷觉细胞位于I层，无害机械感受细胞大多位于II层内侧或上方的白质中。μ阿片类激动剂[D - 丙氨酸(2)，N - 甲基苯丙氨酸(4)，甘氨酸(5) - 醇] - 脑啡肽(DAMGO)使19个受试神经元中的7个发生超极化并伴有电导增加。在应用了纳洛酮的神经元中，这种超极化被逆转。DAMGO还降低了13个神经元的自发突触后电位频率，其中7个神经元也被DAMGO超极化。7个超极化神经元中有5个是伤害性感受神经元，对热和机械性有害刺激均有反应，而另外2个对缓慢的无害轻刷刺激有反应。这些结果表明，全细胞、紧密封接记录所采集的大鼠I层和II层神经元群体与猫和猴中用尖锐电极记录所发现的相似。它们还进一步表明，DAMGO使一部分同时接受热和机械伤害感受器输入的伤害性感受神经元超极化，并且在未被DAMGO超极化的伤害性感受神经元中也能观察到DAMGO的突触前效应。
