Department of Anatomy and Neurosciences, Amsterdam Neuroscience, VU University Medical Centre, Amsterdam, the Netherlands.
Center for Neurogenomics and Cognitive Research, Department of Molecular and Cellular Neurobiology, Amsterdam Neuroscience, VU University, Amsterdam, the Netherlands.
Neuropsychopharmacology. 2019 Nov;44(12):2011-2021. doi: 10.1038/s41386-019-0449-x. Epub 2019 Jun 26.
The role of medial prefrontal cortex (mPFC) in regulating nicotine taking and seeking remains largely unexplored. In this study we took advantage of the high time-resolution of optogenetic intervention by decreasing (Arch3.0) or increasing (ChR2) the activity of neurons in the dorsal and ventral mPFC during 5-s nicotine cue presentations in order to evaluate their contribution to cued nicotine seeking and taking. Wistar rats were trained to self-administer intravenous nicotine in 1 h self-administration sessions twice a day for a minimum of 10 days. Subsequently, dmPFC or vmPFC neuronal activity was modulated during or following presentation of the 5-s nicotine cue, both under extinction and self-administration conditions. We also used in vivo electrophysiology to record the activity of dmPFC neurons during nicotine self-administration and extinction tests. We show that optogenetic inhibition of dmPFC neurons during, but not following, response-contingent presentations of the nicotine cue increased nicotine seeking. We found no effect on nicotine self-administration or on food seeking in an extinction test. We also show that this effect is specific to dmPFC, because optogenetic inhibition of vmPFC had no effect on nicotine seeking and taking. In vivo recordings revealed that dmPFC network neuronal activity was modulated more strongly following nicotine cue presentation in extinction, compared to following nicotine self-administration. Our results strongly suggest that a population of neurons within the dmPFC is involved in encoding the incentive value of nicotine-associated cues.
内侧前额叶皮层(mPFC)在调节尼古丁摄取和寻求方面的作用在很大程度上仍未得到探索。在这项研究中,我们利用光遗传学干预的高时间分辨率,在 5 秒尼古丁线索呈现期间降低(Arch3.0)或增加(ChR2)背侧和腹侧 mPFC 神经元的活性,以评估它们对线索诱导的尼古丁寻求和摄取的贡献。Wistar 大鼠接受训练,每天两次在 1 小时的自我给药会议中自我注射静脉尼古丁,至少 10 天。随后,在消退和自我给药条件下,在 5 秒尼古丁线索呈现期间或之后,调节 dmPFC 或 vmPFC 神经元的活性。我们还使用体内电生理学记录在尼古丁自我给药和消退测试期间 dmPFC 神经元的活动。我们表明,在反应相关的尼古丁线索呈现期间,但不是在反应之后,光遗传抑制 dmPFC 神经元会增加尼古丁寻求。我们没有发现它对尼古丁自我给药或在消退测试中的食物寻求有影响。我们还表明,这种效应是 dmPFC 特有的,因为 vmPFC 的光遗传抑制对尼古丁寻求和摄取没有影响。体内记录显示,与在尼古丁自我给药之后相比,在消退中,dmPFC 网络神经元的活动在尼古丁线索呈现后被更强地调节。我们的结果强烈表明,dmPFC 内的一群神经元参与编码与尼古丁相关线索的激励价值。