Bilateral Inhibition of γ-Aminobutyric Acid Type A Receptor Function within the Basolateral Amygdala Blocked Propofol-induced Amnesia and Activity-regulated Cytoskeletal Protein Expression Inhibition in the Hippocampus
Bilateral Inhibition of γ-Aminobutyric Acid Type A Receptor Function within the Basolateral Amygdala Blocked Propofol-induced Amnesia and Activity-regulated Cytoskeletal Protein Expression Inhibition in the Hippocampus
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DOI：
10.1097/aln.0b013e31818a37c4
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发表时间：
2008-11-01
期刊：
影响因子：
8.8
通讯作者：
Yu, Bu-Wei
中科院分区：
文献类型：
--
作者：
Ren, Yu;Zhang, Fu-Jun;Yu, Bu-Wei
背景资料：有报道称，双侧基底外侧杏仁核复合体（BLA）的损伤阻断了丙泊酚诱导的抑制性回避（1A）训练的遗忘。基于这些结果，作者假设丙泊酚的遗忘作用部分是由于其通过激活BLA γ-氨基丁酸A型受体功能损害海马中的记忆形成。作者确定的活动调节的细胞色素相关蛋白（弧）表达的变化是一个指标1A的记忆formation.Methods：雄性SD大鼠接受双侧注射荷包牡丹碱甲碘（10，50，或100 pmol/0-5亩）或盐水（0-5亩）到BLA。15分钟后，大鼠腹腔注射丙泊酚（25 mg/kg）或生理盐水。5 min后，进行一次试验1A训练。腹腔内注入生理盐水的大鼠作为对照，仅接受BLA内的生理盐水注射。24小时后，测试1A保持潜伏期。结果：最大剂量的甲碘荷包牡丹碱（100 pmol）不仅能阻断丙泊酚引起的记忆障碍，而且能逆转丙泊酚对海马Arc蛋白表达的抑制作用（P < 0.05）。然而，弧的mRNA水平没有表现出显着的变化后，丙泊酚和荷包牡丹碱methiodiaadministration.Conclusions：丙泊酚的健忘效应似乎涉及调制的弧蛋白在海马中的表达，发生通过网络与BLA的相互作用。
Background: It has been reported that bilateral lesions of the basolateral amygdala complex (BLA) blocked propofolinduced amnesia of inhibitory avoidance (1A) training. Based on these results, the authors hypothesized that the amnesia effect of propofol was partly due to its impairment of memory formation in the hippocampus through activating the BLA gamma-aminobutyric acid type A receptor function. The authors determined the changes in activity-regulated cytoskeleton-associated protein (Arc) expression to be an indicator of 1A memory formation.Methods: Male Sprague-Dawley rats received bilateral injection of bicuculline methiodide (10, 50, or 100 pmol/0-5 mu l) or saline (0-5 mu l) into the BLA. Fifteen minutes later, the rats were intraperitoneally injected with either propofol (25 mg/kg) or saline. After 5 min, the one-trial 1A training was conducted. Rats intraperitoneally infused with saline served as controls and only received saline injections into the BLA. Twenty-four hours later, the 1A retention latency was tested. Separate groups of rats treated the same way were killed either 30 min after 1A training for hippocampal Arc mRNA measurement or after 45 min for protein level quantification.Results: The largest dose of bicuculline methiodide (100 pmol) not only blocked the propofol-induced amnesia but also reversed the inhibition effect of propofol on Arc protein expression in the hippocampus (P < 0.05). However, the mRNA level of Arc showed no significant changes after propofol and bicuculline methiodide administration.Conclusions: The amnesic effect of propofol seems to involve the modulation of Arc protein expression in the hippocampus, occurring through a network interaction with the BLA.