Propofol inhibits ketamine-induced c-fos expression in the rat posterior cingulate cortex
Propofol inhibits ketamine-induced c-fos expression in the rat posterior cingulate cortex
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DOI：
10.1097/00000539-199812000-00040
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发表时间：
1998-12-01
影响因子：
5.7
通讯作者：
Shingu, K
中科院分区：
文献类型：
--
作者：
Nagata, A;Nakao, S;Shingu, K
氯胺酮是一种非竞争性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂，具有拟精神病活性。NMDA受体拮抗剂引起后扣带皮层的形态学损伤，这可能是负责其拟精神病作用的脑区。苯二氮卓类药物可通过γ-氨基丁酸A（GABAA）受体激活有效预防这些效应。我们研究了具有GABAA受体激活和NMDA受体抑制活性的丙泊酚对氯胺酮诱导的大鼠后扣带回皮质c-fos表达的影响。持续IV输注丙泊酚或溶媒。15分钟后，腹腔内注射100 mg/kg氯胺酮或等渗氯化钠溶液。2 h后取脑组织，免疫组化法检测c-fos表达。异丙酚显著抑制氯胺酮诱导的c-fos在后扣带回皮质的表达。异丙酚本身不诱导c-fos在该脑区的表达。我们的结论是，异丙酚可能能够抑制氯胺酮诱导的拟精神病活动和神经元损伤。含义：在本研究中，我们证明，临床相关剂量的异丙酚显着抑制氯胺酮诱导的c-fos在大鼠后扣带皮层的表达。这一发现表明，异丙酚可以抑制氯胺酮诱导的拟精神病活动和神经元损伤。
Ketamine, a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, has psychotomimetic activity. NMDA receptor antagonists cause morphological damage in the posterior cingulate cortex, which may be the brain region responsible for their psychotomimetic effects. Benzodiazepines are effective in preventing these effects through gamma-aminobutyric acid A (GABAA) receptor activation. We investigated the effect of propofol, which has both GABAA receptor-activating and NMDA receptor-suppressing activity, on ketamine-induced c-fos expression in the rat posterior cingulate cortex. Propofol or vehicle was continuously infused IV. Fifteen minutes later, 100 mg/kg ketamine or isotonic sodium chloride solution was injected intraperitoneally. Two hours later, brain sections were prepared, and c-fos expression was detected using immunohistochemical methods. Propofol significantly inhibited ketamine-induced c-fos expression in the posterior cingulate cortex. Propofol itself did not induce c-fos expression in this brain region. We conclude that propofol may be able to inhibit ketamine-induced psychotomimetic activity and neuronal damage. Implications: In the present study, we demonstrated that the clinically relevant dose of propofol significantly inhibited ketamine-induced c-fos expression in the rat posterior cingulate cortex. This finding implies that propofol may inhibit ketamine-induced psychotomimetic activity and neuronal damage.