Theunissen Eef L, van Kroonenburgh Marinus J P G, van Deursen Jeroen A, Blom-Coenjaerts Ciska, Ramaekers Johannes G
Experimental Psychopharmacology Unit, Department of Neurocognition, Faculty of Psychology, University of Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands.
Psychopharmacology (Berl). 2006 Jul;187(1):95-102. doi: 10.1007/s00213-006-0406-3. Epub 2006 May 23.
First- and second-generation antihistamines are known to produce different degrees of sedation. However, a few studies have shown that the H1-antagonist fexofenadine produces mild stimulating effects. One hypothesis suggests that this is due to fexofenadine producing an increase in dopamine levels by blocking the dopamine transporter.
In this study, it was investigated whether a high dose of fexofenadine blocks the dopamine transporter in the striatum. In addition, the effect of fexofenadine on cognitive performance and motor impulsivity was investigated.
Sixteen healthy subjects were given either placebo or fexofenadine 360 mg. The binding potential of N-w-fluoropropyl-2beta-carbomethoxy-3beta-[4-iodophenyl] nortropane ([123I]FP-CIT) was measured using single-photon emission computed tomography (SPECT). Cognitive performance was measured in 40 subjects (20 placebo, 20 fexofenadine) using a digit symbol substitution test (DSST) and a stop signal task. In addition, subjective and physiological effects of fexofenadine were observed.
The SPECT data demonstrated that there was no difference in the binding potential of FP-CIT at the dopamine transporter in the striatum between the placebo- and fexofenadine-treated subjects. The behavioral results showed that fexofenadine improved performance on the DSST at T (max) of the drug. Fexofenadine did not affect motor impulsivity, subjective experience, or physiological measures.
No evidence was provided to support the hypothesis that fexofenadine stimulates performance by blocking the dopamine transporter. The behavioral data suggest that a high dose of fexofenadine can stimulate performance in cognitive tasks.
已知第一代和第二代抗组胺药会产生不同程度的镇静作用。然而，一些研究表明，H1 拮抗剂非索非那定会产生轻度刺激作用。一种假说认为，这是由于非索非那定通过阻断多巴胺转运体导致多巴胺水平升高。
在本研究中，调查了高剂量非索非那定是否会阻断纹状体中的多巴胺转运体。此外，还研究了非索非那定对认知表现和运动冲动性的影响。
16 名健康受试者分别服用安慰剂或 360 毫克非索非那定。使用单光子发射计算机断层扫描（SPECT）测量 N-ω-氟丙基-2β-甲氧基羰基-3β-[4-碘苯基]去甲托烷（[123I]FP-CIT）的结合潜能。使用数字符号替换测试（DSST）和停止信号任务对 40 名受试者（20 名服用安慰剂，20 名服用非索非那定）的认知表现进行测量。此外，还观察了非索非那定的主观和生理效应。
SPECT 数据表明，服用安慰剂和非索非那定的受试者纹状体中多巴胺转运体处 FP-CIT 的结合潜能没有差异。行为学结果显示，非索非那定在药物达峰时间（T(max)）时改善了 DSST 的表现。非索非那定不影响运动冲动性、主观体验或生理指标。
没有证据支持非索非那定通过阻断多巴胺转运体来刺激表现的假说。行为学数据表明，高剂量非索非那定可刺激认知任务中的表现。
