Potency ratios of morphine and morphine-6beta-glucuronide analgesia elicited from the periaqueductal gray, locus coeruleus or rostral ventromedial medulla of rats.
Potency ratios of morphine and morphine-6beta-glucuronide analgesia elicited from the periaqueductal gray, locus coeruleus or rostral ventromedial medulla of rats.
复制标题
吗啡和吗啡-6β-葡萄糖醛酸从大鼠导水管周围灰质、蓝斑或头端腹内侧延髓引起的镇痛效价比。
DOI：
10.1016/s0006-8993(98)00520-4
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发表时间：
1998
期刊：
影响因子：
2.9
通讯作者：
Bodnar,RJ
中科院分区：
文献类型：
--
作者：
Krzanowska,EK;Rossi,GC;Pasternak,GW;Bodnar,RJ
本研究探讨了吗啡和吗啡-6 β-葡萄糖醛酸苷（M6 G）在甩尾和跳跃试验中的镇痛作用在中脑导水管周围灰质、蓝斑或延髓头端腹内侧区的效力是否不同。吗啡和M6 G显着和剂量依赖性地引起镇痛的伤害性测试从每个网站。在M6 G的效力中观察到位点特异性差异，但在两个测试中未观察到吗啡镇痛。中脑导水管周围灰质放置物在甩尾（吗啡：2.1 μg，M6 G：0.2 μg）和跳跃（吗啡：2.2 μg，M6 G：0.4 μg）试验中显示镇痛ED 50，其效力比分别为12.9和6.5。在甩尾（吗啡：1.7 μg，M6 G：0.1 μg）和跳跃（吗啡：3.4 μg，M6 G：0.2 μg）实验中，蓝斑放置显示镇痛ED 50，其效力比分别为15.9和15.1。在甩尾（吗啡：1.4 μg，M6 G：0.06 μg）和跳跃（吗啡：1.9 μg，M6 G：0.08 μg）试验中，头侧腹内侧放置的镇痛ED_（50）均为21.9。延髓头端腹内侧区对M6 G的镇痛敏感性更高可能是由于药效学（莫尔-1基因的剪接变体）和/或药代动力学（脂溶性）因素。
The present study examined whether morphine and morphine-6β-glucuronide (M6G) analgesia on the tail-flick and jump tests differed in potency in the periaqueductal gray, the locus coeruleus or the rostral ventromedial medulla. Morphine and M6G significantly and dose-dependently elicited analgesia on both nociceptive tests from each site. Site-specific differences were observed in the potency of M6G, but not morphine analgesia on both tests. Periaqueductal gray placements displayed analgesic ED50son the tail-flick (morphine: 2.1 μg, M6G: 0.2 μg) and jump (morphine: 2.2 μg, M6G: 0.4 μg) tests with respective potency ratios of 12.9 and 6.5. Locus coeruleus placements displayed analgesic ED50son the tail-flick (morphine: 1.7 μg, M6G: 0.1 μg) and jump (morphine: 3.4 μg, M6G: 0.2 μg) tests with respective potency ratios of 15.9 and 15.1. Rostral ventromedial placements displayed analgesic ED50son the tail-flick (morphine: 1.4 μg, M6G: 0.06 μg) and jump (morphine: 1.9 μg, M6G: 0.08 μg) tests with potency ratios of 21.9 on both tests. The greater analgesic sensitivity of the rostral ventromedial medulla to M6G may be due to either pharmacodynamic (splice variants of the MOR-1 gene) and/or pharmacokinetic (lipid solubility) factors.