Schomburg E D, Steffens H
Physiologisches Institut der Universität, Göttingen, Germany.
Exp Brain Res. 1995;103(3):333-43. doi: 10.1007/BF00241493.
The effects of L-DOPA, naloxone, and the opioids (D-Ala2,N-Me-Phe4,Gly5-ol)-enkephalin (DAGO) and D-Ser2-Leu-enkephalin-Thr6 (DSLET) on spinal motor rhythm generation were compared in anemically decapitated high spinal cats. After premedication with nialamide, DOPA caused the well-known, slow rhythmic motor activity with a locomotor pattern. The cycle duration of the evoked rhythm was usually between 3.9 and 5.0 s. The opioids DAGO and DSLET, injected intravenously (1.2-2 mg/kg) or suffused over the lumbar spinal cord (10(-3)-10(-4) M in Ringer's solution), severely depressed the DOPA-induced rhythmic activity, sometimes completely abolishing efferent motor activity. Naloxone (0.5-1 mg/kg i.v.) exerted different rhythm-facilitating effects, depending on the experimental condition. In the acute phase after spinalization, without paralysis and without nialamide and DOPA, naloxone induced rhythmic movements with a main frequency of 1.2-2 Hz. In the same preparation with paralysis, naloxone induced a rhythmic motor activity with a distinctly higher frequency (main range 4.3-5.8 Hz). After premedication with nialamide and DOPA, naloxone facilitated or, if a rhythm was absent, induced the slow-frequency DOPA type of rhythm. Given after i.v. or topical opioid application, naloxone antagonized the rhythm-depressing action of the opioid and caused an additional facilitation of rhythmic activity. Dopa and naloxone facilitated the long-latency, segmental reflex pathways from flexor reflex afferents (FRA), while the opioids depressed them. The short-latency FRA pathways were depressed by DOPA and opioids but were facilitated by naloxone. The influence of the different drugs on spinal motor rhythm generation is discussed in relation to their influence on short- and long-latency segmental pathways from FRA. If the rhythm generation induced by DOPA is based on the release of the long-latency FRA pathways, as has been proposed before, the rhythm-depressing action of opioids may be due to the suppression of these pathways, and the particular rhythm-generating function of naloxone may be related to its facilitation of short- and long-latency FRA pathways.
在贫血断头的高位脊髓猫中，比较了左旋多巴、纳洛酮以及阿片类药物（D-丙氨酸2，N-甲基苯丙氨酸4，甘氨酸5-醇）-脑啡肽（DAGO）和D-丝氨酸2-亮氨酸-脑啡肽-苏氨酸6（DSLET）对脊髓运动节律产生的影响。在用尼亚酰胺预处理后，左旋多巴引起了众所周知的、具有运动模式的缓慢节律性运动活动。诱发节律的周期持续时间通常在3.9至5.0秒之间。静脉注射（1.2 - 2毫克/千克）或在腰段脊髓上灌注（林格氏液中浓度为10⁻³ - 10⁻⁴摩尔）的阿片类药物DAGO和DSLET，严重抑制了左旋多巴诱导的节律性活动，有时完全消除传出运动活动。纳洛酮（静脉注射0.5 - 1毫克/千克）根据实验条件产生不同的节律促进作用。在脊髓横断后的急性期，无瘫痪且未用尼亚酰胺和左旋多巴时，纳洛酮诱导出主要频率为1.2 - 2赫兹的节律性运动。在相同的有瘫痪的制备中，纳洛酮诱导出频率明显更高（主要范围为4.3 - 5.8赫兹）的节律性运动活动。在用尼亚酰胺和左旋多巴预处理后，纳洛酮促进了或在无节律时诱导出左旋多巴类型的慢频率节律。在静脉注射或局部应用阿片类药物后给予纳洛酮，它拮抗了阿片类药物的节律抑制作用，并额外促进了节律性活动。左旋多巴和纳洛酮促进了来自屈肌反射传入纤维（FRA）的长潜伏期节段反射通路，而阿片类药物则抑制了它们。短潜伏期FRA通路被左旋多巴和阿片类药物抑制，但被纳洛酮促进。讨论了不同药物对脊髓运动节律产生的影响与其对来自FRA的短潜伏期和长潜伏期节段通路的影响之间的关系。如果如之前所提出的，左旋多巴诱导的节律产生是基于长潜伏期FRA通路的释放，那么阿片类药物的节律抑制作用可能是由于这些通路的抑制，而纳洛酮独特的节律产生功能可能与其对短潜伏期和长潜伏期FRA通路的促进作用有关。
