Department of Alcohol, Drugs and Addiction, National Institute for Health and Welfare , Helsinki , Finland.
Front Psychiatry. 2015 Jan 20;6:1. doi: 10.3389/fpsyt.2015.00001. eCollection 2015.
The purpose of the present study was to investigate the role of ventral pallidal opioidergic mechanisms in the control of ethanol intake by studying the effects of acute administration of morphine on the levels of GABA, glutamate, and dopamine in the ventral pallidum. The study was conducted using the alcohol-preferring Alko Alcohol (AA) and alcohol-avoiding Alko Non-Alcohol (ANA) rat lines that have well-documented differences in their voluntary ethanol intake and brain opioidergic systems. Therefore, examination of neurobiological differences between the lines is supposed to help to identify the neuronal mechanisms underlying ethanol intake, since selection pressure is assumed gradually to lead to enrichment of alleles promoting high or low ethanol intake, respectively. The effects of an acute dose of morphine (1 or 10 mg/kg s.c.) on the extracellular levels of GABA and glutamate in the ventral pallidum were monitored with in vivo microdialysis. The concentrations of GABA and glutamate in the dialyzates were determined with a high performance liquid chromatography system using fluorescent detection, while electrochemical detection was used for dopamine. The levels of glutamate in the rats injected with morphine 1 mg/kg were significantly above the levels found in the controls and in the rats receiving morphine 10 mg/kg. Morphine 10 mg/kg also increased the levels of dopamine. Morphine could not, however, modify the levels of GABA. The rat lines did not differ in any of the effects of morphine. The data suggest that the glutamatergic and dopaminergic systems in the ventral pallidum may mediate some effects of morphine. Since there were no differences between the AA and ANA lines, the basic hypothesis underlying the use of the genetic animal model suggests that the effects of morphine detected probably do not underlie the different intake of ethanol by the lines and contribute to the control of ethanol intake in these animals.
本研究旨在通过研究急性给予吗啡对腹侧苍白球中 GABA、谷氨酸和多巴胺水平的影响，探讨腹侧苍白球阿片能机制在乙醇摄入控制中的作用。该研究使用了具有明确差异的酒精偏好 Alko Alcohol (AA) 和酒精回避 Alko Non-Alcohol (ANA) 大鼠品系，它们在自愿性乙醇摄入和大脑阿片系统方面存在差异。因此，检查品系之间的神经生物学差异应该有助于确定乙醇摄入的神经元机制，因为选择压力被认为会逐渐导致促进高或低乙醇摄入的等位基因的富集。使用活体微透析监测急性给予吗啡（1 或 10mg/kg sc）对腹侧苍白球中 GABA 和谷氨酸的细胞外水平的影响。使用高效液相色谱系统结合荧光检测测定透析液中 GABA 和谷氨酸的浓度，而电化学检测则用于多巴胺。给予吗啡 1mg/kg 的大鼠的谷氨酸浓度明显高于对照组和给予吗啡 10mg/kg 的大鼠。吗啡 10mg/kg 还增加了多巴胺的水平。然而，吗啡不能改变 GABA 的水平。吗啡对两种大鼠品系的作用没有差异。这些数据表明，腹侧苍白球中的谷氨酸能和多巴胺能系统可能介导吗啡的一些作用。由于 AA 和 ANA 品系之间没有差异，使用遗传动物模型的基本假设表明，检测到的吗啡的作用可能不是导致这些品系摄入不同量乙醇的原因，并且在这些动物中有助于控制乙醇摄入。
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