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貨號：G180，R180

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

國內渠(qu)道(dao)現貨商：靶點科技

論(lun)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(qing)春期酗酒(jiu)非常普(pu)遍(bian)，盡(jin)管越來越多的(de)(de)證(zheng)據表明其對(dui)內側前(qian)額葉(xie)皮層 （mPFC） 調節行(xing)為(wei)(wei)靈活性(xing)(xing)(xing)(xing)相關(guan)的(de)(de)行(xing)為(wei)(wei)有(you)長期影響。在本研究(jiu)中(zhong)，雄性(xing)(xing)(xing)(xing)和(he)雌性(xing)(xing)(xing)(xing)大鼠(shu)通過蒸氣吸入接(jie)受(shou)了青(qing)春期間歇性(xing)(xing)(xing)(xing)乙(yi)醇（AIE）暴(bao)露。衰老到(dao)(dao)成年后，使用逆行(xing)珠標(biao)記和(he)病毒標(biao)記來識別 mPFC 前(qian)邊緣區域(yu) （PrL） 中(zhong)投(tou)射(she)(she)到(dao)(dao)特定皮質下(xia)靶標(biao)的(de)(de)神經(jing)(jing)元(yuan)(yuan)群。來自 PrL 切片中(zhong)珠子標(biao)記神經(jing)(jing)元(yuan)(yuan)的(de)(de)電生理記錄(lu)顯示(shi)，AIE 不會改變(bian)(bian)投(tou)射(she)(she)到(dao)(dao) NAc 或(huo) BLA 的(de)(de) PrL 神經(jing)(jing)元(yuan)(yuan)的(de)(de)內在興奮性(xing)(xing)(xing)(xing)。同樣，自發性(xing)(xing)(xing)(xing)抑制(zhi)性(xing)(xing)(xing)(xing)和(he)興奮性(xing)(xing)(xing)(xing)突(tu)(tu)觸后電流(liu)的(de)(de)記錄(lu)顯示(shi)，沒有(you)AIE誘導(dao)的(de)(de)突(tu)(tu)觸驅動對(dui)任何一個投(tou)射(she)(she)神經(jing)(jing)元(yuan)(yuan)群體(ti)的(de)(de)變(bian)(bian)化(hua)。相比之下(xia)，AIE 暴(bao)露與(yu)多巴胺受(shou)體(ti) 1 （D1） 的(de)(de)丟失有(you)關(guan)，但(dan)多巴胺受(shou)體(ti) 2 （D2） 沒有(you)變(bian)(bian)化(hua)，調節兩個投(tou)射(she)(she)神經(jing)(jing)元(yuan)(yuan)群的(de)(de)誘發放電。最(zui)后，投(tou)射(she)(she)到(dao)(dao)伏隔核 （NAc） 的(de)(de)病毒標(biao)記的(de)(de) PrL 神經(jing)(jing)元(yuan)(yuan)的(de)(de)近端和(he)頂端樹突(tu)(tu)簇的(de)(de)共聚焦(jiao)成像顯示(shi) AIE 不會改變(bian)(bian)樹突(tu)(tu)棘的(de)(de)密度。總之，這(zhe)些(xie)觀察結果提供了證(zheng)據，證(zheng)明 AIE 暴(bao)露導(dao)致(zhi) D1 受(shou)體(ti)對(dui) PrL 輸入的(de)(de)調節破(po)壞，這(zhe)些(xie)區域(yu)至少與(yu) AIE 誘導(dao)的(de)(de)行(xing)為(wei)(wei)控(kong)制(zhi)長期變(bian)(bian)化(hua)有(you)關(guan)。

英文摘要(yao)：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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