Juvenile Obesity Enhances Emotional Memory and Amygdala Plasticity through Glucocorticoids
Juvenile Obesity Enhances Emotional Memory and Amygdala Plasticity through Glucocorticoids
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DOI：
10.1523/jneurosci.3122-14.2015
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发表时间：
2015-03-04
影响因子：
5.3
通讯作者：
Ferreira, Guillaume
中科院分区：
文献类型：
--
作者：
Boitard, Chloe;Maroun, Mouna;Ferreira, Guillaume
除了代谢和心血管疾病外，肥胖还与不良认知和情绪结果相关。它在青春期的日益流行尤其令人担忧，因为最近的证据表明，肥胖会影响海马体在这一发育时期的功能。青春期是杏仁核和下丘脑-垂体-肾上腺（HPA）应激轴成熟的决定性时期，两者都是终身认知和情感处理所必需的。然而，关于青春期肥胖对杏仁核功能影响的数据很少。因此，我们在大鼠中评估青少年高脂饮食（HFD）诱导的肥胖是否会改变杏仁核依赖的情绪记忆，以及它是否依赖于HPA轴失调。从断奶到成年暴露于HFD，即，覆盖青春期，增强长期的情感记忆，通过气味不适和音调休克协会评估。青少年HFD还增强了杏仁核基底外侧复合体（BLA）的情绪诱导的神经元激活，这与血浆皮质酮释放延长相关。仅限于成年期的HFD暴露不会改变所有这些参数，表明青春期是HFD诱导的肥胖影响的脆弱时期。最后，夸张的情绪记忆和青少年HFD后BLA突触可塑性减轻糖皮质激素受体拮抗剂。总之，我们的研究结果表明，青少年HFD改变HPA轴的反应性，导致杏仁核依赖的突触和记忆过程的增强。青春期是杏仁核功能对饮食诱导的肥胖影响的易感性增加的时期。
In addition to metabolic and cardiovascular disorders, obesity is associated with adverse cognitive and emotional outcomes. Its growing prevalence during adolescence is particularly alarming since recent evidence indicates that obesity can affect hippocampal function during this developmental period. Adolescence is a decisive period for maturation of the amygdala and the hypothalamic-pituitary-adrenal (HPA) stress axis, both required for lifelong cognitive and emotional processing. However, little data are available on the impact of obesity during adolescence on amygdala function. Herein, we therefore evaluate in rats whether juvenile high-fat diet (HFD)-induced obesity alters amygdala-dependent emotional memory and whether it depends on HPA axis deregulation. Exposure to HFD from weaning to adulthood, i.e., covering adolescence, enhances long-term emotional memories as assessed by odor-malaise and tone-shock associations. Juvenile HFD also enhances emotion-induced neuronal activation of the basolateral complex of the amygdala (BLA), which correlates with protracted plasma corticosterone release. HFD exposure restricted to adulthood does not modify all these parameters, indicating adolescence is a vulnerable period to the effects of HFD-induced obesity. Finally, exaggerated emotional memory and BLA synaptic plasticity after juvenile HFD are alleviated by a glucocorticoid receptor antagonist. Altogether, our results demonstrate that juvenile HFD alters HPA axis reactivity leading to an enhancement of amygdala-dependent synaptic and memory processes. Adolescence represents a period of increased susceptibility to the effects of diet-induced obesity on amygdala function.