Morgan Celia J A, Rossell Susan L, Pepper Fiona, Smart James, Blackburn James, Brandner Brigitta, Curran H Valerie
Clinical Psychopharmacology Unit, University College London, London WC1E 6BT, United Kingdom.
Biol Psychiatry. 2006 Feb 1;59(3):265-72. doi: 10.1016/j.biopsych.2005.06.018. Epub 2005 Sep 2.
Ketamine is used acutely as a model of schizophrenia. It has been suggested that chronic ketamine may also mimic aspects of this disorder, in particular impaired cognitive function. As semantic processing deficits are considered central to cognitive impairments in schizophrenia, this study aimed to characterize semantic impairments following both acute and chronic ketamine.
We examined the acute effects of two doses of ketamine (Experiment 1) using a double-blind, placebo-controlled, independent group design with 48 volunteers. Ketamine's chronic effects (Experiment 2) were explored in 16 ketamine users and 16 poly-drug controls. A semantic priming task with a frequency (high and low) and stimulus onset asynchrony (SOA: short-200 msec, long-750 msec) manipulation was used.
In Experiment 1, acute ketamine produced inverse priming at the long SOA. In Experiment 2, ketamine users showed inverse priming for low-frequency words at the long SOA compared to poly-drug controls.
The inverse priming effect at the long SOA induced by acute ketamine was indicative of controlled processing impairments. In ketamine users, there was also an indication of controlled processing impairments. Decreased priming for low-frequency words suggested that long-term ketamine abuse results in damage to the semantic store.
氯胺酮被急性用作精神分裂症模型。有人提出，慢性氯胺酮也可能模拟这种疾病的某些方面，特别是认知功能受损。由于语义加工缺陷被认为是精神分裂症认知障碍的核心，本研究旨在描述急性和慢性氯胺酮使用后的语义损伤情况。
我们采用双盲、安慰剂对照、独立组设计，对48名志愿者进行了两剂氯胺酮的急性效应研究（实验1）。在16名氯胺酮使用者和16名多药使用者对照组中探究了氯胺酮的慢性效应（实验2）。使用了一个语义启动任务，该任务对频率（高和低）以及刺激开始时间间隔（SOA：短-200毫秒，长-750毫秒）进行了操控。
在实验1中，急性氯胺酮在长SOA时产生了负启动效应。在实验2中，与多药使用者对照组相比，氯胺酮使用者在长SOA时对低频词表现出负启动效应。
急性氯胺酮在长SOA时诱导的负启动效应表明存在控制性加工障碍。在氯胺酮使用者中，也有控制性加工障碍的迹象。低频词启动效应的降低表明长期滥用氯胺酮会导致语义存储受损。
