用户名: 密码: 验证码:
An examination of the effects of subthalamic nucleus inhibition or -opioid receptor stimulation on food-directed motivation in the non-deprived rat
详细信息查看全文 | 推荐本文 |
摘要
The subthalamic nucleus (STN) serves important functions in regulating movement, cognition, and motivation and is connected with cortical and basal ganglia circuits that process reward and reinforcement. In order to further examine the role of the STN on motivation toward food in non-deprived rats, these experiments studied the effects of pharmacological inhibition or -opioid receptor stimulation of the STN on the 2-h intake of a sweetened fat diet, the amount of work exerted to earn sucrose on a progressive ratio 2 (PR-2) schedule of reinforcement, and performance on a differential reinforcement of low-rate responding (DRL) schedule for sucrose reward. Separate behavioral groups (N = 6-9) were tested following bilateral inhibition of the STN with the GABAA receptor agonist muscimol (at 0-5 ng/0.5 l/side) or following -opioid receptor stimulation with the agonist D-Ala2, N-MePhe4, Gly-ol-enkephalin (DAMGO; at 0, 0.025 or 0.25 g/0.5 l/side). Although STN inhibition increased ambulatory behavior during 2-h feeding sessions, it did not significantly alter intake of the sweetened fat diet. STN inhibition also did not affect the breakpoint for sucrose pellets during a 1-h PR-2 reinforcement schedule or impact the number of reinforcers earned on a 1-h DRL-20 s reinforcement schedule in non-deprived rats. In contrast, STN -opioid receptor stimulation significantly increased feeding on the palatable diet and reduced the reinforcers earned on a DRL-20 schedule, although DAMGO microinfusions had no effect on PR-2 performance. These data suggest that STN inhibition does not enhance incentive motivation for food in the absence of food restriction and that STN -opioid receptors play an important and unique role in motivational processes.

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700