Parolaro D, Massi P, Patrini G, Rubino T, Parenti M, Gori E
Institute of Pharmacology, Faculty of Sciences, School of Medicine, University of Milan, Italy.
Pharmacol Biochem Behav. 1991 Mar;38(3):569-73. doi: 10.1016/0091-3057(91)90015-t.
Intracerebroventricular injection of pertussis toxin (PTX, 1 microgram/rat) six days before the hot plate test abolished analgesia induced by central morphine. The toxin did not affect analgesia evoked by central neurotensin or ASU 1-7 eel calcitonin. PTX pretreatment also attenuated footshock-induced analgesia (FSIA) delivered to all four paws. When the shock was restricted to the front paws, PTX consistently lowered postshock tail flick latencies, but did not reduce analgesia resulting from shock delivered to the hind paws. It thus appears that PTX-sensitive G-proteins are an essential transduction step needed to initiate the molecular events underlying opiate analgesia evoked by either morphine or shock. In contrast, the signal transduction mechanism subsequent to the stimulation of neurotensin or calcitonin receptors, and to the nonopiate FSIA, appears not to involve PTX-sensitive G-proteins.
在热板试验前六天，向大鼠脑室内注射百日咳毒素（PTX，1微克/大鼠）可消除中枢给予吗啡诱导的镇痛作用。该毒素不影响中枢给予神经降压素或鳗鱼降钙素ASU 1-7诱导的镇痛作用。PTX预处理还减弱了施加于所有四只爪子的足部电击诱导的镇痛作用（FSIA）。当电击仅限于前爪时，PTX持续缩短电击后甩尾潜伏期，但不降低后爪电击所致的镇痛作用。因此，似乎对PTX敏感的G蛋白是启动吗啡或电击诱发的阿片类镇痛作用基础分子事件所需的关键转导步骤。相比之下，神经降压素或降钙素受体刺激后以及非阿片类FSIA后的信号转导机制似乎不涉及对PTX敏感的G蛋白。
