目标:近交系小鼠品系在介导糖和脂肪摄入以及条件风味偏好(CFP)的药理学上有所不同。C57BL/6、BALB/c和SWR近交系小鼠对多巴胺(DA)D1、阿片样物质和毒蕈碱受体对蔗糖的拮抗作用差异敏感,糖精或脂肪摄入量,对DA来说,阿片类药物获得蔗糖-CFP的毒蕈碱和N-甲基-D-天冬氨酸(NMDA)受体拮抗作用。DAD1、阿片样物质和NMDA受体拮抗剂在BALB/c和SWR小鼠中差异改变脂肪(Intralipid)-CFP。本研究检查了纳曲酮是否,SCH23390或MK-801改变了C57BL/6小鼠中脂质-CFP的获得和表达。方法:在获取中,受食物限制的雄性C57BL/6小鼠组接受媒介物,纳曲酮(1,5mg/kg),SCH23390(50,200nmol/kg)或MK-801(100,200μg/kg),然后进行10次训练,其中小鼠交替食用两种新型风味的5%(CS)和0.5%(CS-)内脂溶液。随后进行了六个两瓶CS选择测试,将两种口味混合在0.5%Intralipid中,无需注射。在表达式中,C57BL/6小鼠在没有注射的情况下进行了10次训练,然后在载体后30分钟进行两瓶CS选择测试,纳曲酮(1,5mg/kg),SCH23390(200,800nmol/kg)或MK-801(100,200μg/kg)。结果:纳曲酮后,C57BL/6小鼠的脂肪-CFP采集显着降低,SCH23390和MK-801。纳曲酮同样降低了脂肪-CFP的表达,C57BL/6小鼠中的SCH23390和MK-801。讨论:C57BL/6小鼠对DAD1、阿片样物质和NMDA拮抗剂在脂肪-CFP的表达相对于糖-CFP更敏感,但相对于糖-CFP,在获得脂肪-CFP时对DAD1和NMDA拮抗剂的敏感性较低。
Objectives: Inbred mouse strains differ in the pharmacology mediating sugar and fat intake and conditioned flavor preferences (CFP). C57BL/6, BALB/c and SWR inbred mice are differentially sensitive to dopamine (DA) D1, opioid and muscarinic receptor antagonism of sucrose, saccharin or fat intake, and to DA, opioid, muscarinic and N-methyl-D-aspartate (NMDA) receptor antagonism of acquisition of sucrose-CFP. DA D1, opioid and NMDA receptor antagonists differentially alter fat (Intralipid)-CFP in BALB/c and SWR mice. The present study examined whether naltrexone,
SCH23390 or MK-801 altered acquisition and expression of Intralipid-CFP in C57BL/6 mice.Methods: In acquisition, groups of male food-restricted C57BL/6 mice received vehicle, naltrexone (1, 5 mg/kg),
SCH23390 (50, 200 nmol/kg) or MK-801 (100, 200 μg/kg) before 10 training sessions in which mice alternately consumed two novel-flavored 5% (CS+) and 0.5% (CS-) Intralipid solutions. Six two-bottle CS choice tests followed with both flavors mixed in 0.5% Intralipid without injections. In expression, C57BL/6 mice underwent the 10 training sessions without injections followed by two-bottle CS choice tests 30 min following vehicle, naltrexone (1, 5 mg/kg),
SCH23390 (200, 800 nmol/kg) or MK-801 (100, 200 μg/kg).Results: Fat-CFP acquisition in C57BL/6 mice was significantly though marginally reduced following naltrexone,
SCH23390 and MK-801. Fat-CFP expression was similarly reduced by naltrexone,
SCH23390 and MK-801 in C57BL/6 mice. Discussion: C57BL/6 mice were more sensitive to DA D1, opioid and NMDA antagonists in the expression of fat-CFP relative to sugar-CFP, but were less sensitive to DA D1 and NMDA antagonists in the acquisition of fat-CFP relative to sugar-CFP.