Traore M, Maitte M, Delerm B, Roy J C, Sequeira H
Laboratoire de Neurosciences du Comportement, Université de Lille 1, Villeneuve d'Ascq, France.
J Physiol Paris. 1998 Feb;92(1):17-23. doi: 10.1016/S0928-4257(98)80018-1.
By analogy with supraspinal and spinal inhibitory controls of pain, it was hypothesized that an opioid mechanism could be involved in the bulbar inhibitory control of the electrodermal activity. This activity was evoked as skin potential responses on the footpads of 13 cats by the central tegmental field stimulation (control responses) and inhibited by the simultaneous stimulation of bulbar reticular formation (experimental responses). Then, naloxone, an opioid peptide antagonist, was injected intravenously or intrathecally and its effects were analyzed on both control and experimental responses. Intravenous injections of naloxone increased significantly the amplitude of experimental responses from 6 to 12 min after the injection and had no effect on the amplitude of control responses. Intrathecal injections of naloxone induced significant increases of amplitude of experimental responses from 6 to 42 min after the injection. These results showed that a spinal opioid peptide link could be involved in bulbar inhibition mechanisms of electrodermal activity.
通过与疼痛的脊髓上和脊髓抑制控制进行类比,有人推测阿片类机制可能参与了延髓对皮肤电活动的抑制控制。在13只猫的脚垫上,通过中央被盖区刺激诱发这种活动作为皮肤电位反应(对照反应),并通过同时刺激延髓网状结构来抑制(实验反应)。然后,静脉内或鞘内注射阿片肽拮抗剂纳洛酮,并分析其对对照反应和实验反应的影响。静脉注射纳洛酮后6至12分钟,实验反应的幅度显著增加,而对对照反应的幅度没有影响。鞘内注射纳洛酮后6至42分钟,实验反应的幅度显著增加。这些结果表明,脊髓阿片肽联系可能参与了皮肤电活动的延髓抑制机制。