Department of Anaesthesiology, Ludwig-Maximilians University, Munich, Germany.
Anesthesiology. 2011 Jun;114(6):1380-8. doi: 10.1097/ALN.0b013e31821c120e.
Propofol is associated with postoperative mood alterations and induces a higher incidence of dreaming compared with other general anesthetics. These effects might be mediated by propofol's inhibitory action on fatty acid amide hydrolase, the enzyme that degrades the endocannabinoid anandamide. Because propofol is also associated with a higher incidence of traumatic memories from perioperative awareness and intensive care unit treatment and the endocannabinoid system is involved in regulating memory consolidation of emotional experiences, the authors investigated whether propofol, at anesthetic doses, modulates memory consolidation via an activation of the endocannabinoid system.
Male Sprague-Dawley rats were trained on an inhibitory avoidance task in which they received an inescapable foot shock upon entering the dark compartment of the apparatus. Drugs were administered intraperitoneally immediately or 30, 90, or 180 min after training. On the retention test 48 h later, the latency to reenter the dark compartment was recorded and taken as a measure of memory retention.
The anesthetic doses of propofol administered after training significantly increased latencies of 48-h inhibitory avoidance performance (483.4 ± 181.3, 432.89 ± 214.06, 300 and 350 mg/kg, respectively; mean ± SD) compared with the corresponding vehicle group (325.33 ± 221.22, mean ± SD), which is indicative of stronger memory consolidation in propofol treated rats. Administration of a nonimpairing dose of the cannabinoid receptor antagonist rimonabant blocked the memory enhancement induced by propofol (123.39 ± 133.10, mean ± SD). Delayed administration of propofol 90 and 180 min after training or immediate posttraining administration of the benzodiazepine midazolam or the barbiturate pentobarbital did not significantly alter retention.
These findings indicate that propofol, in contrast to other commonly used sedatives, enhances emotional memory consolidation when administered immediately after a stressful event by enhancing endocannabinoid signaling.
与其他全身麻醉药物相比,丙泊酚会引起术后情绪改变和更高的梦境发生率。这些作用可能是通过丙泊酚对脂肪酸酰胺水解酶的抑制作用介导的,该酶可降解内源性大麻素大麻酰胺。由于丙泊酚还与围手术期意识和重症监护治疗期间创伤性记忆的发生率较高有关,并且内源性大麻素系统参与调节情绪体验的记忆巩固,作者研究了在麻醉剂量下,丙泊酚是否通过激活内源性大麻素系统来调节记忆巩固。
雄性 Sprague-Dawley 大鼠在抑制性回避任务中接受训练,当它们进入仪器的黑暗隔间时会受到不可避免的足部电击。药物在训练后立即或 30、90 或 180 分钟时通过腹腔内给药。在 48 小时后的保留测试中,记录重新进入黑暗隔间的潜伏期,并作为记忆保留的测量值。
与相应的载体组(325.33 ± 221.22,均值 ± SD)相比,训练后给予麻醉剂量的丙泊酚显著增加了 48 小时抑制性回避表现的潜伏期(分别为 483.4 ± 181.3、432.89 ± 214.06、300 和 350mg/kg,均值 ± SD),这表明丙泊酚处理的大鼠中记忆巩固更强。大麻素受体拮抗剂利莫那班的非损伤剂量给药阻断了丙泊酚诱导的记忆增强(123.39 ± 133.10,均值 ± SD)。训练后 90 分钟和 180 分钟延迟给予丙泊酚或立即给予苯二氮䓬类咪达唑仑或巴比妥类戊巴比妥钠均不会显著改变保留。
这些发现表明,与其他常用镇静剂相比,丙泊酚在应激事件后立即给予时,通过增强内源性大麻素信号来增强情绪记忆巩固,从而增强情绪记忆巩固。