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首页> 外文会议>Conference on Neural Imaging and Sensing;Society of Photo-Optical Instrumentation Engineers >Optical Imaging of Prefrontal Deficits Induced by Cocaine: Neurons vs Dopamine D2-receptor Expressing Neurons
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Optical Imaging of Prefrontal Deficits Induced by Cocaine: Neurons vs Dopamine D2-receptor Expressing Neurons

机译：可卡因诱发的前额叶光学成像：神经元与多巴胺D2受体表达神经元。

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Deficits in the medial prefrontal cortex (mPFC) function play a crucial role in promoting compulsive cocaine use. Thisdysfunction might result from cocaine’s effects on neurons possibly including modification of the expression of thedopamine type 2 receptors (D2r). However, studies on D2r function have been hindered by relatively low receptorexpression in mPFC and low detection sensitivity. To tackle this problem, we developed a workflow to optically imageD2r through enhancing visualization of GFP fluorescence in a D2r-expressing transgenic mouse model. Two groups ofanimals were used: group 1 was treated daily by saline (0.1cc/100g, i.p.) and group 2 received cocaine (30mg/kg, i.p.)for 2 weeks. Following 1-day withdrawal, their brains were fixed and processed. The brain sections underwentimmunostaining and ex vivo imaging using a confocal fluorescence microscope to capture co-registered fluorescencelabeling of both neurons (NeuN) and D2r-expressing neurons (GFP). These images were montaged to cover a large fieldof view of the mPFC to quantify the changes in the count of neurons and D2r-expressing neurons. Our results show thatchronic cocaine exposure results in 34.7%±5.7% decrease in neurons but a 44.7%±13.2% increase of D2r expressingneurons in the mPFC compared to saline treated group. Additionally, in-vivo Ca~(2+) imaging of D2r-expressing neurons inthe mPFC revealed cocaine’s effects on the prefrontal response to the stimulation at the VTA. These changes mightunderlie the hypofrontality observed in human studies and exacerbate the loss of control associated with chronic cocaineuse.
机译：内侧前额叶皮质（MPFC）功能中的缺陷在促进强迫性可卡因使用方面发挥着至关重要的作用。这 可卡因的功能障碍可能是可卡因对神经元的影响可能包括改变表达的 多巴胺2型受体（D2R）。然而，对D2R功能的研究已经受到相对低的受体的阻碍 MPFC中的表达和低检测灵敏度。为了解决这个问题，我们开发了一个光学映像的工作流程 D2R通过增强D2R表达转基因小鼠模型中GFP荧光的可视化。两组 使用动物：第1组每天通过盐水处理（0.1cc / 100g，i.p.）和第2组接受可卡因（30mg / kg，i.p.） 2周。在撤回1天后，将其大脑固定并加工。大脑切片接受了 使用共焦荧光显微镜捕获共登记荧光的免疫染色和离体成像 标记神经元（NeUN）和D2R表达神经元（GFP）。这些图像被砍成覆盖大场 MPFC的看法量化神经元数和D2R表达神经元数的变化。我们的结果表明 慢性可卡因暴露导致神经元减少34.7％±5.7％，但表达D2R的增加44.7％±13.2％ MPFC中的神经元与盐水处理组相比。另外，D2R表达神经元的体内Ca〜（2+）成像 MPFC揭示了可卡因对VTA刺激的前额外反应的影响。这些变化可能 在人类研究中观察到的缺口性，加剧了与慢性可卡因相关的对照的丧失 使用。

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