Rat dorsal horn nociceptive-specific neurons are more sensitive than wide dynamic range neurons to depression by immobilizing doses of volatile anesthetics: an effect partially reversed by the opioid receptor antagonist naloxone.
Rat dorsal horn nociceptive-specific neurons are more sensitive than wide dynamic range neurons to depression by immobilizing doses of volatile anesthetics: an effect partially reversed by the opioid receptor antagonist naloxone.
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DOI：
10.1213/ane.0b013e3181a9770f
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发表时间：
2009-08
影响因子：
5.7
通讯作者：
Antognini JF
中科院分区：
文献类型：
--
作者：
Barter LS;Carstens EE;Jinks SL;Antognini JF
挥发性麻醉剂在脊髓内产生不动的机制和作用部位尚不清楚。很少有研究直接比较麻醉对具有特定功能特征的神经元的影响，这些神经元介导脊髓内伤害性信息的传递。成年雄性大鼠麻醉后，准备进行腰背角的细胞外单单位记录。在最小肺泡麻醉浓度（MAC）为0.8和1.2的氟烷或异氟烷条件下，研究人员鉴定了伤害特异性（NS）和宽动态范围（WDR）神经元，并评估了毒热诱发的神经元尖峰率。在另一组中，对0.8、1.2 MAC氟烷和1.2 MAC氟烷加IV纳洛酮（0.1 mg/kg）时的NS神经元的毒热诱发反应进行评估。当氟烷浓度从0.8℃升高到1.2℃时，NS神经元（n=9）的热诱发反应从827±122（平均±SE）降低到343±48 (p < 0.05)，而WDR神经元（n=9）的热诱发反应从617±79降低到547±78 （p < 0.05）。当异氟醚浓度从0.8到1.2 MAC时，NS神经元（n=9）的热诱发反应从890±339个峰/min降低到188±97个峰/min (p < 0.05)，而WDR神经元（n=9）的热诱发反应从576±132个峰/min降低到601±119个峰/min。在另一个单独的组中，当氟烷从0.8到1.2 MAC增加时，NS神经元的反应从282±60增加到74±32 spike /min (p < 0.05)，静脉给纳洛酮使热诱发反应增加到155±46 spike /min （p < 0.05）。氟烷和异氟烷在大鼠腰背角周围增加，可抑制NS神经元，但不抑制WDR神经元。这种抑制，至少与氟烷，可以部分逆转阿片类拮抗剂纳洛酮。鉴于阿片受体不太可能参与挥发性麻醉剂产生不动的机制，这表明，尽管神经元抑制是相当大的，并且与不动的产生同时发生，但它可能在这种麻醉终点的产生中不起主要作用。
The mechanism and site of action within the spinal cord by which volatile anesthetics produce immobility are not well understood. Little work has been done directly comparing anesthetic effects on neurons with specific functional characteristics that mediate transfer of nociceptive information within the spinal cord. Adult male rats were anesthetized and prepared for extracellular single-unit recordings from the lumbar dorsal horn. Nociceptive-specific (NS) and wide dynamic range (WDR) neurons were identified and noxious-heat evoked neuronal spike rates evaluated at 0.8 and 1.2 minimum alveolar anesthetic concentration (MAC) halothane or isoflurane. In another group, noxious-heat evoked responses from NS neurons were evaluated at 0.8, 1.2 MAC halothane, and 1.2 MAC halothane plus IV naloxone (0.1 mg/kg). Increasing halothane from 0.8 to 1.2 MAC reduced the heat-evoked neuronal responses of NS neurons (n=9) from 827 ± 122 (mean ± SE) to 343 ± 48 spikes/ min (p < 0.05) but not WDR neurons (n=9), 617 ± 79 to 547 ± 78 spikes/min. Increasing isoflurane from 0.8 to 1.2 MAC reduced the heat-evoked neuronal response of NS neurons (n=9) from 890 ± 339 to 188 ± 97 spikes/ min (p < 0.05), but did not alter the response of WDR neurons (n=9) in which evoked spike rate went from 576 ± 132 to 601 ± 119 spikes/min. In a separate group, the response from NS neurons went from 282 ± 60 to 74 ± 32 spikes/min (p < 0.05) when halothane was increased from 0.8 to 1.2 MAC. Intravenous administration naloxone increased the heat-evoked response to 155 ± 46 spikes/min (p < 0.05). NS but not WDR neurons in the lumbar dorsal horn are depressed by peri-MAC increases of halothane and isoflurane. This depression, at least with halothane, can be partially reversed by the opioid antagonist naloxone. Given that opioid receptors are not likely involved in the mechanisms by which volatile anesthetics produce immobility, this suggests that, although the neuronal depression is of substantial magnitude and occurs concurrent to the production of immobility, it may not play a major role in the production of this anesthetic end-point.
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影响因子：
1.7
作者：
Machado, CE;Dyson, DH;Grant Maxie, M
通讯作者：
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作者：
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