Parent Marise B
Neuroscience Institute, Department of Psychology, Georgia State University, PO Box 5030, Atlanta, GA 30303-5030, United States.
Physiol Behav. 2016 Aug 1;162:112-9. doi: 10.1016/j.physbeh.2016.03.036. Epub 2016 Apr 13.
There is a large gap in our understanding of how top-down cognitive processes, such as memory, influence energy intake. Similarly, there is limited knowledge regarding how the brain controls the timing of meals and meal frequency. Understanding how cognition influences ingestive behavior and how the brain controls meal frequency will provide a more complete explanation of the neural mechanisms that regulate energy intake and may also increase our knowledge of the factors that contribute to diet-induced obesity. We hypothesize that dorsal hippocampal neurons, which are critical for memory of personal experiences (i.e., episodic memory), form a memory of a meal, inhibit meal onset during the period following a meal, and limit the amount ingested at the next meal. In support, we describe evidence from human research suggesting that episodic memory of a meal inhibits intake and review data from human and non-human animals showing that impaired hippocampal function is associated with increased intake. We then describe evidence from our laboratory showing that inactivation of dorsal hippocampal neurons decreases the interval between sucrose meals and increases intake at the next meal. We also describe our evidence suggesting that sweet orosensation is sufficient to induce synaptic plasticity in dorsal hippocampal neurons and raise the possibility that impaired dorsal hippocampal function and episodic memory deficits contribute to the development and/or maintenance of diet-induced obesity. Finally, we raise some critical questions that need to be addressed in future research.
我们对诸如记忆等自上而下的认知过程如何影响能量摄入的理解存在很大差距。同样,关于大脑如何控制进餐时间和进餐频率的知识也很有限。了解认知如何影响摄食行为以及大脑如何控制进餐频率,将为调节能量摄入的神经机制提供更完整的解释,还可能增加我们对导致饮食诱导性肥胖的因素的认识。我们假设,对个人经历记忆(即情景记忆)至关重要的背侧海马神经元形成进餐记忆,在进餐后的时间段抑制进餐开始,并限制下一餐的摄入量。作为支持,我们描述了来自人类研究的证据,表明进餐的情景记忆会抑制摄入量,并回顾了来自人类和非人类动物的数据,这些数据表明海马功能受损与摄入量增加有关。然后,我们描述了来自我们实验室的证据,表明背侧海马神经元失活会缩短蔗糖餐之间的间隔,并增加下一餐的摄入量。我们还描述了我们的证据,表明甜味口腔感觉足以诱导背侧海马神经元的突触可塑性,并提出背侧海马功能受损和情景记忆缺陷可能导致饮食诱导性肥胖的发展和/或维持。最后,我们提出了一些未来研究需要解决的关键问题。