Unique responses of limbic met-enkephalin systems to low and high doses of methamphetamine
Unique responses of limbic met-enkephalin systems to low and high doses of methamphetamine
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DOI：
10.1016/s0006-8993(01)02514-8
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发表时间：
2001-06-29
期刊：
影响因子：
2.9
通讯作者：
Hanson, GR
中科院分区：
文献类型：
--
作者：
Alburges, ME;Keefe, KA;Hanson, GR
单次低剂量（0.5 mg/kg）或高剂量（10 mg/kg）的甲基苯丙胺（METH）显著改变了与部分（但不是全部）大脑边缘结构相关的脑啡肽（M-Enk）系统。两种治疗都不影响药物暴露后3小时任何边缘区域的M-Enk水平；然而，给药12小时后，0.5 mg/kg甲基安非他明降低了伏隔核壳（NAs）和额叶皮质（FrCx）中该肽的组织含量。这与这种治疗对前纹状体区域的影响相似。大剂量甲基安非他明增加了大鼠额叶皮层和前纹状体的M-Enk含量，但对伏隔核壳没有影响。24 h时，甲基苯丙胺对前纹状体的影响减弱，但伏隔核壳内低剂量和高剂量甲基苯丙胺处理后M-Enk水平仍呈下降趋势。在伏隔核（NAc）核心检测的任何时间点上，M-Enk水平均未发生变化。一般来说，用低剂量或高剂量的甲基安非他明治疗会导致边缘系统中M-Enk的组织水平发生明显的区域性选择性变化。这些变化似乎是由多巴胺（DA） D-2和D-1受体激活介导的。(C) 2001 Elsevier Science B.V.版权所有
A single administration of a low (0.5 mg/kg) or high (10 mg/kg) dose of methamphetamine (METH) significantly altered the met-enkephalin (M-Enk) systems associated with some, but not all, limbic structures examined. Neither treatment influenced M-Enk levels 3 h after drug exposure in any limbic region studied; however, 12 h after drug administration, 0.5 mg/kg of METH reduced the tissue content of this peptide in both the nucleus accumbens shell (NAs) and the frontal cortex (FrCx). This was similar to the effect of this treatment on the anterior striatal region. In contrast, the high dose of METH increased M-Enk content in the frontal cortex and anterior striatum (AS), but had no effect in the nucleus accumbens shell. By 24 h, the effects of METH in the anterior striatum subsided, but decreases in M-Enk levels were still observed after both the low- and the high-dose METH treatments in the nucleus accumbens shell. The levels of M-Enk were not changed at any of the time points examined in the core of the nucleus accumbens (NAc). In general, treatment with a low or high dose of METH causes distinct and regional selective changes in the tissue levels of M-Enk in the limbic system. These changes appear to be mediated by dopamine (DA) D-2 and D-1 receptor activation. (C) 2001 Elsevier Science B.V. All rights reserved.