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Lumafluor绿色Green Retrobeads登2022年期刊Addiction Neuroscience

更新时间:2024-02-07   点击次数:247次

品牌:Lumafluor

货号:G180,R180

名称:Green Retrobeads™ (100 µl),Red Retrobeads™ (100 µl)

国内渠道现货商:靶点科技

论文题目Adolescent alcohol exposure reduces dopamine 1 receptor modulation of prelimbic neurons projecting to the nucleus accumbens and basolateral amygdala

期刊Addiction Neuroscience Volume 4, December 2022, 100044

中文摘要:青春期酗酒非常普遍,尽管越来越多的证据表明其对内侧前额叶皮层 (mPFC) 调节行为灵活性相关的行为有长期影响。在本研究中,雄性和雌性大鼠通过蒸气吸入接受了青春期间歇性乙醇(AIE)暴露。衰老到成年后,使用逆行珠标记和病毒标记来识别 mPFC 前边缘区域 (PrL) 中投射到特定皮质下靶标的神经元群。来自 PrL 切片中珠子标记神经元的电生理记录显示,AIE 不会改变投射到 NAc 或 BLA 的 PrL 神经元的内在兴奋性。同样,自发性抑制性和兴奋性突触后电流的记录显示,没有AIE诱导的突触驱动对任何一个投射神经元群体的变化。相比之下,AIE 暴露与多巴胺受体 1 (D1) 的丢失有关,但多巴胺受体 2 (D2) 没有变化,调节两个投射神经元群的诱发放电。最后,投射到伏隔核 (NAc) 的病毒标记的 PrL 神经元的近端和顶端树突簇的共聚焦成像显示 AIE 不会改变树突棘的密度。总之,这些观察结果提供了证据,证明 AIE 暴露导致 D1 受体对 PrL 输入的调节破坏,这些区域至少与 AIE 诱导的行为控制长期变化有关。

英文摘要:Binge drinking during adolescence is highly prevalent despite increasing evidence of its long-term impact on behaviors associated with modulation of behavioral flexibility by the medial prefrontal cortex (mPFC). In the present study, male and female rats underwent adolescent intermittent ethanol (AIE) exposure by vapor inhalation. After aging to adulthood, retrograde bead labelling and viral tagging were used to identify populations of neurons in the prelimbic region (PrL) of the mPFC that project to specific subcortical targets. Electrophysiological recording from bead-labelled neurons in PrL slices revealed that AIE did not alter the intrinsic excitability of PrL neurons that projected to either the NAc or the BLA. Similarly, recordings of spontaneous inhibitory and excitatory post-synaptic currents revealed no AIE-induced changes in synaptic drive onto either population of projection neurons. In contrast, AIE exposure was associated with a loss of dopamine receptor 1 (D1), but no change in dopamine receptor 2 (D2), modulation of evoked firing of both populations of projection neurons. Lastly, confocal imaging of proximal and apical dendritic tufts of viral-labelled PrL neurons that projected to the nucleus accumbens (NAc) revealed AIE did not alter the density of dendritic spines. Together, these observations provide evidence that AIE exposure results in disruption of D1 receptor modulation of PrL inputs to at least two major subcortical target regions that have been implicated in AIE-induced long-term changes in behavioral control.

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