品牌：Lumafluor

貨號：G180，R180

名稱：Green Retrobeads™ (100 µl)供給，Red Retrobeads™ (100 µl)

國內渠道現貨商：靶點科技

論文題目：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，盡管越來越多的證據表明其對內側前額葉皮層 （mPFC） 調節(jié)行為靈活性相關的行為有長期影響具體而言。在本研究中，雄性和雌性大鼠通過蒸氣吸入接受了青春期間歇性乙醇（AIE）暴露智慧與合力。衰老到成年后喜愛，使用逆行珠標記和病毒標記來識別 mPFC 前邊緣區(qū)域 （PrL） 中投射到特定皮質下靶標的神經元群。來自 PrL 切片中珠子標記神經元的電生理記錄顯示數據顯示，AIE 不會改變投射到 NAc 或 BLA 的 PrL 神經元的內在興奮性高質量。同樣，自發(fā)性抑制性和興奮性突觸后電流的記錄顯示記得牢，沒有AIE誘導的突觸驅動對任何一個投射神經元群體的變化註入了新的力量。相比之下，AIE 暴露與多巴胺受體 1 （D1） 的丟失有關更多可能性，但多巴胺受體 2 （D2） 沒有變化去創新，調節(jié)兩個投射神經元群的誘發(fā)放電足夠的實力。最后，投射到伏隔核 （NAc） 的病毒標記的 PrL 神經元的近端和頂端樹突簇的共聚焦成像顯示 AIE 不會改變樹突棘的密度又進了一步《喾N場景？傊嘣阵w系，這些觀察結果提供了證據規劃，證明 AIE 暴露導致 D1 受體對 PrL 輸入的調節(jié)破壞，這些區(qū)域至少與 AIE 誘導的行為控制長期變化有關深度。

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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