Taheri Saeid, Xun Zhu, See Ronald E, Joseph Jane E, Reichel Carmela M
Department of Pharmaceutical Sciences, University of South Florida, Tampa FL 33612.
Department of Neurosciences, Medical University of South Carolina, Charleston SC 29425.
Brain Res. 2016 Jul 1;1642:497-504. doi: 10.1016/j.brainres.2016.04.040. Epub 2016 Apr 18.
Neuroimaging studies in psychostimulant addicts have reported functional neural activity changes in brain regions involved in relapse. However, the difference between the effects of the psychostimulants methamphetamine and cocaine on neuronal activity in a similar setting not been clarified. Since studies in humans are limited by the inability to study the initial impact of psychostimulant drugs, we addressed this issue in a rat model.
Here, we report methamphetamine and cocaine-induced blood-oxygen-level dependent (BOLD) signal change using functional magnetic resonance imaging (fMRI) in rats receiving drug for the first time during the imaging session.
Twenty-three male Long Evans rats underwent fMRI imaging and received an intravenous infusion of methamphetamine, cocaine, or saline. Anatomical and pharmacological fMRI (pfMRI) were performed on a 7T BioSpec dedicated research MR scanner under isoflurane gas (1.5-2%). After collecting baseline data for 10min, rats received drug over the next 10min for a total 40min scan time. Data were then preprocessed and statistically analyzed in anatomically defined regions of interest (ROIs) that have been implicated in persistent drug seeking and relapse.
Methamphetamine during the imaging session resulted in a sustained negative BOLD signal change in key regions of the relapse circuit, except for the prefrontal cortex. In contrast, cocaine evoked a positive or unchanged BOLD signal in these same regions. In all of the investigated ROIs, there were no changes in BOLD signal following saline.
Acute methamphetamine and cocaine have distinct patterns of functional activity as measured by pfMRI.
对精神兴奋剂成瘾者的神经影像学研究报告了参与复发的脑区功能神经活动变化。然而，在类似情况下，精神兴奋剂甲基苯丙胺和可卡因对神经元活动的影响差异尚未明确。由于人体研究受到无法研究精神兴奋剂药物初始影响的限制，我们在大鼠模型中解决了这个问题。
在此，我们报告在成像过程中首次接受药物的大鼠中，使用功能磁共振成像（fMRI）测量甲基苯丙胺和可卡因诱导的血氧水平依赖（BOLD）信号变化。
23只雄性Long Evans大鼠接受fMRI成像，并接受静脉注射甲基苯丙胺、可卡因或生理盐水。在7T BioSpec专用研究磁共振扫描仪上，在异氟烷气体（1.5 - 2%）下进行解剖学和药理功能磁共振成像（pfMRI）。在收集10分钟的基线数据后，大鼠在接下来的10分钟内接受药物注射，总扫描时间为40分钟。然后对数据进行预处理，并在与持续药物寻求和复发相关的解剖学定义的感兴趣区域（ROI）中进行统计分析。
在成像过程中，甲基苯丙胺导致复发回路关键区域的BOLD信号持续负向变化，但前额叶皮质除外。相比之下，可卡因在这些相同区域引起正向或不变的BOLD信号。在所有研究的ROI中，注射生理盐水后BOLD信号没有变化。
通过pfMRI测量，急性甲基苯丙胺和可卡因具有不同的功能活动模式。
