Kelsey John E, Willmore Ellen J
Department of Psychology and Program in Neuroscience, Bates College, Lewiston, ME 04240, USA.
Behav Neurosci. 2006 Jun;120(3):600-11. doi: 10.1037/0735-7044.120.3.600.
Electrolytic lesions of the medial core of the nucleus accumbens (NAc) in male Long-Evans rats increased spontaneous locomotion, enhanced the locomotor stimulating effect of acute 5.0 mg/kg cocaine, enhanced the development and subsequent expression of locomotor sensitization produced by repeated injections of 0.4 mg/kg nicotine but not 7.5 mg/kg cocaine, and enhanced the expression of conditioned locomotion. Given that 6-hydroxydopamine lesions of the NAc typically have effects on locomotor-related processes that are opposite of those produced by electrolytic and excitotoxic lesions, these data are consistent with a hypothesis that the NAc output, especially from the core, inhibits a variety of such processes and that the DA input to the NAc enhances these processes by inhibiting this inhibitory output.
对雄性Long-Evans大鼠伏隔核（NAc）内侧核心进行电解损伤后，自发运动增加，急性注射5.0毫克/千克可卡因所产生的运动刺激作用增强，重复注射0.4毫克/千克尼古丁而非7.5毫克/千克可卡因所产生的运动敏化的发展及后续表达增强，且条件性运动的表达增强。鉴于NAc的6-羟基多巴胺损伤通常对与运动相关的过程产生的影响与电解损伤和兴奋性毒性损伤所产生的影响相反，这些数据与以下假设一致：NAc的输出，尤其是来自核心的输出，会抑制多种此类过程，而向NAc的多巴胺输入通过抑制这种抑制性输出增强了这些过程。
