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Frustrative nonreward: Chemogenetic inactivation of the central amygdala abolishes the effect of reward downshift without affecting alcohol intake.
Neurobiology of Learning and Memory ( IF 2.2 ) Pub Date : 2020-01-27 , DOI: 10.1016/j.nlm.2020.107173
Sara Guarino 1 , Shannon E Conrad 1 , Mauricio R Papini 1
Affiliation  

The role of the central amygdala (CeA) in the adjustment to a 32-to-2% sucrose downshift in the consummatory successive negative contrast (cSNC) task and in a free-choice 10% alcohol-water preference task (PT) was studied using chemogenetic inactivation. cSNC is a model of frustrative nonreward that enhances alcohol consumption. In Experiment 1, sessions 1-10 involved 5-min access to 32% sucrose and sessions 11-12 involved access to 2% sucrose. Vehicle or clozapine N-oxide (CNO; 1 or 3 mg/kg, ip), used later to activate the inhibitory designer receptor, was administered 30 min before sessions 11-12. There was no evidence that CNO affected consummatory behavior after the sucrose downshift. In Experiment 2, all animals received an infusion of the inhibitory designer receptor hM4D(Gi) into the CeA. After recovery, animals received access to either 32% or 2% sucrose on sessions 1-10, followed by 2% sucrose on sessions 11-12. Immediately after each 5-min sucrose session, animals received a 2-bottle, 1-h PT with 10% alcohol and water. CNO (3 mg/kg, ip) or vehicle was administered 30 min before sessions 11-12. CeA inactivation prior to sucrose downshift eliminated the cSNC effect, which was observed in vehicle controls. However, there was no evidence that CeA inactivation affected preference for 10% alcohol over water. These results support the hypothesis that CeA activity is critical for cSNC effect, an outcome consistent with the view that the amygdala plays a central role in frustrative nonreward.

中文翻译:

令人沮丧的无奖赏:中央杏仁核的化学成因失活消除了奖励降档的影响,而不影响酒精的摄入。

研究了中央杏仁核(CeA)在渐进式负性反差(cSNC)任务和自由选择的10%酒精-水偏爱任务(PT)中将蔗糖降低32%调整为2%的作用。使用化学发生灭活。cSNC是令人沮丧的无奖赏的模型,可增加饮酒量。在实验1中,课程1-10涉及5分钟获取32%蔗糖,而课程11-12涉及涉及2%蔗糖。在第11-12节之前30分钟,施用了溶媒或氯氮平N-氧化物(CNO; 1或3 mg / kg,腹膜内),随后用于激活抑制性设计者受体。没有证据表明蔗糖下降后CNO影响了消费行为。在实验2中,所有动物都接受了抑制性设计受体hM4D(Gi)到CeA的输注。恢复后 在第1-10节中,动物接受32%或2%蔗糖的摄取,然后在第11-12节中接受2%蔗糖的摄取。每次蔗糖5分钟灌胃后,立即给动物灌胃2瓶,1小时PT和10%酒精和水。在第11至12节前30分钟施用CNO(3 mg / kg,ip)或载体。蔗糖降档之前CeA失活消除了cSNC效应,这在媒介物对照中观察到。但是,没有证据表明CeA失活会影响人们对10%的酒精而非水的偏好。这些结果支持了CeA活性对于cSNC效应至关重要的假设,这一结果与杏仁核在令人沮丧的不奖励中起着核心作用的观点一致。与10%酒精和水的PT 1小时。在第11至12节前30分钟施用CNO(3 mg / kg,ip)或载体。蔗糖降档之前CeA失活消除了cSNC效应,这在媒介物对照中观察到。但是,没有证据表明CeA失活会影响人们对10%的酒精而非水的偏好。这些结果支持了CeA活性对于cSNC效应至关重要的假设,这一结果与杏仁核在令人沮丧的不奖励中起着核心作用的观点一致。与10%酒精和水的PT 1小时。在第11至12节前30分钟施用CNO(3 mg / kg,ip)或载体。蔗糖降档之前CeA失活消除了cSNC效应,这在媒介物对照中观察到。但是,没有证据表明CeA失活会影响人们对10%的酒精而非水的偏好。这些结果支持了CeA活性对于cSNC效应至关重要的假设,这一结果与杏仁核在令人沮丧的不奖励中起着核心作用的观点一致。
更新日期:2020-01-27
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