Department of Anesthesiology, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA.
Department of Anesthesiology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Sci Rep. 2016 Sep 15;6:33538. doi: 10.1038/srep33538.
How general anesthesia interferes with sensory processing to cause amnesia remains unclear. Here, we show that activation of a learning-associated immediate early gene in rat olfactory cortices is uninterrupted by propofol, an intravenous general anesthetic with putative actions on the inhibitory GABAA receptors. Once learned under anesthesia, a novel odor can no longer re-activate the same high-level transcription programming during subsequent conscious relearning. Behavioral tests indicate that the animals' ability to consciously relearn a pure odorant, first experienced under general anesthesia, is indeed compromised. In contrast, when a mixture of two novel odorants is first experienced under anesthesia and then relearned consciously in pairs with one of the components, the animals show a deficit in relearning only the component but not the mixture. Our results reveal a previously unknown mechanism of unconscious memory due to irreplaceable neuronal commitment under general anesthesia and support the notion that general anesthesia acts at stages beyond cellular coding to disrupt sensory integration for higher-order association.
全麻如何干扰感觉处理从而导致遗忘仍不清楚。在这里，我们表明，在静脉全身麻醉药异丙酚的作用下，大鼠嗅觉皮层中的学习相关的早期基因的激活未受干扰，异丙酚可能作用于抑制性 GABA 受体。一旦在麻醉下学习，新气味在随后的清醒再学习中就不能再重新激活相同的高级转录编程。行为测试表明，动物在全麻下首次体验纯气味后有意识地重新学习的能力确实受到了损害。相比之下，当两种新气味混合物首先在麻醉下体验，然后与其中一种成分在成对的情况下有意识地重新学习时，动物仅在重新学习成分而不是混合物时表现出缺陷。我们的结果揭示了一种由于全麻下神经元的不可替代性而导致的无意识记忆的先前未知机制，并支持全麻作用于细胞编码以外的阶段以破坏感觉整合的观点，用于更高阶的联想。
