品牌：Lumafluor

貨號(hào)：G180，R180

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

國(guó)內(nèi)渠道現(xiàn)貨商：靶點(diǎn)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(lái)越多的證據(jù)表明其對(duì)內(nèi)側(cè)前額葉皮層 （mPFC） 調(diào)節(jié)行為靈活性相關(guān)的行為有長(zhǎng)期影響。在本研究中，雄性和雌性大鼠通過(guò)蒸氣吸入接受了青春期間歇性乙醇（AIE）暴露。衰老到成年后，使用逆行珠標(biāo)記和病毒標(biāo)記來(lái)識(shí)別 mPFC 前邊緣區(qū)域 （PrL） 中投射到特定皮質(zhì)下靶標(biāo)的神經(jīng)元群。來(lái)自 PrL 切片中珠子標(biāo)記神經(jīng)元的電生理記錄顯示，AIE 不會(huì)改變投射到 NAc 或 BLA 的 PrL 神經(jīng)元的內(nèi)在興奮性。同樣，自發(fā)性抑制性和興奮性突觸后電流的記錄顯示，沒(méi)有AIE誘導(dǎo)的突觸驅(qū)動(dòng)對(duì)任何一個(gè)投射神經(jīng)元群體的變化。相比之下，AIE 暴露與多巴胺受體 1 （D1） 的丟失有關(guān)，但多巴胺受體 2 （D2） 沒(méi)有變化，調(diào)節(jié)兩個(gè)投射神經(jīng)元群的誘發(fā)放電。最后，投射到伏隔核 （NAc） 的病毒標(biāo)記的 PrL 神經(jīng)元的近端和頂端樹(shù)突簇的共聚焦成像顯示 AIE 不會(huì)改變樹(shù)突棘的密度。總之，這些觀察結(jié)果提供了證據(jù)，證明 AIE 暴露導(dǎo)致 D1 受體對(duì) PrL 輸入的調(diào)節(jié)破壞，這些區(qū)域至少與 AIE 誘導(dǎo)的行為控制長(zhǎng)期變化有關(guān)。

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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