Associative mechanisms underlying the function of satiety cues in the control of energy intake and appetitive behavior.
Associative mechanisms underlying the function of satiety cues in the control of energy intake and appetitive behavior.
复制标题
饱足感线索在控制能量摄入和食欲行为中的作用背后的关联机制。
DOI：
10.1016/j.physbeh.2018.03.017
复制
发表时间：
2018
影响因子：
2.9
通讯作者：
Davidson,TerryL
中科院分区：
文献类型：
--
作者：
Jones,Sabrina;Sample,CamilleH;Hargrave,SaraL;Davidson,TerryL
虽然之前的研究已经确定了许多可以作为潜在饱腹感信号的代谢、神经和激素事件，但使饱腹感信号抑制寻求食物和饮食行为的机制仍然不清楚。在这里，我们研究了这样一种观点，即饱腹感信号的抑制能力至少部分源自它们发出信号的能力，即食物和食物相关的刺激不会随之而来强化进食后的后果。从这个角度来看，嵌入饱足感线索的信号关系定义了巴甫洛夫条件反射中所谓的“串行特征否定”（sFN）辨别问题。在这个问题中，在没有强化的试验中，“负面特征”提示先于“目标”提示的呈现。相反，当没有出现负面特征提示时，目标会在试验中得到强化。饱腹感线索可以被视为与负面特征线索的功能平行，因为它们发出信号，表明与食物相关的目标线索何时将不被强化。我们对老鼠进行了两项实验，评估饱腹感信号是否像负面特征刺激一样发挥作用。实验 1 将饱腹感线索明确预训练为负面特征刺激、不相关刺激，或者在其充当负面特征刺激的能力减弱的条件下。饱足感线索控制对这些实验意外事件高度敏感，接受 sFN 预训练的大鼠表现出最佳表现。这种 sFN 预训练也转移到了后续训练中，以提高另一个具有外部和内部负面特征线索的 sFN 问题的性能。我们还发现，饱足感线索的歧视性控制阻碍了外部线索控制的发展。实验 2 评估了当饱腹感线索被训练为负面特征刺激时，已知会通过外部负面特征线索（即维持西方饮食）损害 sFN 表现的操作是否也会损害 sFN 表现。结果表明，与标准食物相比，WD 摄入对 sFN 性能的损害与两种类型的刺激相似。这些实验提供的证据表明，关联机制（如潜在的 sFN 表现）与饱腹感线索对食欲行为的控制有关。
While previous research has identified a number of metabolic, neural, and hormonal events that could serve as potential satiety signals, the mechanisms that enable satiety signals to suppress food-seeking and eating behavior remain poorly specified. Here we investigate the idea that the inhibitory power of satiety signals is derived, at least in part, from their ability to signal that foods and food-related stimuli will not be followed by reinforcing postingestive consequences. Viewed in this way, the signaling relationship in which satiety cues are embedded defines what is known in Pavlovian conditioning as a “serial feature negative” (sFN) discrimination problem. In this problem a “negative feature” cue precedes the presentation of a “target” cue on trials without reinforcement. In contrast, the target is reinforced on trials when the negative feature cue is not presented. Satiety cues can be seen as paralleling the function of negative feature cues in that they signal when food-related target cues will be nonreinforced. We conducted two experiments with rats that assessed if satiety signals functioned like negative feature stimuli. Experiment 1 explicitly pretrained satiety cues as negative feature stimuli, irrelevant stimuli, or under conditions where their ability to serve as negative feature stimuli would be attenuated. Control by satiety cues was highly sensitive to these experimental contingencies, with the best performance exhibited by rats given sFN pretraining. This sFN pretraining also transferred to enhance performance during subsequent training on another sFN problem with both external and internal negative feature cues. We also found that discriminative control by satiety cues blocked the development of that control by external cues. Experiment 2 evaluated whether a manipulation known to impair sFN performance with external negative feature cues (i.e., maintenance on a western diet) would also impair sFN performance when satiety cues were trained as negative feature stimuli. The results showed that compared to standard chow, WD intake impaired sFN performance similarly with both types of stimuli. These experiments provide evidence that an associative mechanism, like that underlying sFN performance, is involved with the control of appetitive behavior by satiety cues.