Regulatory interactions of stress and reward on rat forebrain opioidergic and GABAergic circuitry.
Regulatory interactions of stress and reward on rat forebrain opioidergic and GABAergic circuitry.
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DOI：
10.3109/10253890.2010.531331
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发表时间：
2011-03
期刊：
影响因子：
--
通讯作者：
Ulrich-Lai YM
中科院分区：
文献类型：
--
作者：
Christiansen AM;Herman JP;Ulrich-Lai YM
美味食物的摄入减少了压力反应，这表明人们可能会将这种“安慰”食物作为缓解压力的自我药物。美味食物缓解压力的机制尚不清楚，但可能存在于前脑奖励和压力调节回路的交汇处。前脑阿片能和γ -氨基丁酸（GABA）能信号对于奖励和压力调节都是至关重要的，这表明这些系统是通过美味食物介导压力缓解的主要候选系统。因此，本研究旨在确定1)可口的“安慰”食物如何改变应激诱导的奖励和应激神经回路中抑制性神经递质mRNA表达的变化，以及2)确定可能支持安慰食物介导的应激减轻的候选大脑区域。我们使用可口的“零食”模型与慢性可变应激模型相结合，然后进行原位杂交，以确定前脑前阿片样物质和谷氨酸脱羧酶（GAD） mRNA的水平。这些数据表明，杏仁核、纹状体和下丘脑内的区域是在吃了美味零食后调节下丘脑-垂体-肾上腺轴（HPA）缓冲的潜在区域。具体而言，仅食用可口零食可降低终纹前床核和伏隔核脑啡肽mRNA的表达，降低终纹后床核GAD65 mRNA的表达。慢性应激单独增加下丘脑、伏隔核、杏仁核和海马中的脑啡肽mRNA；伏隔核肌啡肽mRNA表达升高；下丘脑前部和终纹床核GAD65 mRNA表达升高；下丘脑背侧GAD65 mRNA表达减少。重要的是，美味食物的摄入阻止了下丘脑亚区、终纹床核和伏隔核中应激诱导的基因表达变化。总的来说，这些数据表明，大脑奖励和压力通路之间存在复杂的相互作用，美味的零食可以减轻慢性压力引起的许多神经化学变化。
Palatable food intake reduces stress responses, suggesting that individuals may consume such “comfort” food as self-medication for stress relief. The mechanism by which palatable foods provide stress relief is not known, but likely lies at the intersection of forebrain reward and stress regulatory circuits. Forebrain opioidergic and gamma-aminobutyric acid (GABA)ergic signaling is critical for both reward and stress regulation suggesting that these systems are prime candidates for mediating stress relief by palatable foods. Thus, the current study aimed to determine 1) how palatable “comfort” food alters stress induced changes in the mRNA expression of inhibitory neurotransmitters in reward and stress neurocircuitry, and 2) identify candidate brain regions that may underlie comfort food-mediated stress reduction. We used a model of palatable “snacking” in combination with a model of chronic variable stress followed by in situ hybridization to determine forebrain levels of pro-opioid and glutamic acid decarboxylase (GAD) mRNA. The data identify regions within the extended amygdala, striatum, and hypothalamus as potential regions for mediating hypothalamic-pituitary-adrenal axis (HPA)-buffering following palatable snacking. Specifically, palatable snacking alone decreased enkephalin mRNA expression in the anterior bed nucleus of the stria terminalis and the nucleus accumbens, as well as decreasing GAD65 mRNA in the posterior bed nucleus of the stria terminalis. Chronic stress alone increased enkephalin mRNA in the hypothalamus, nucleus accumbens, amygdala, and hippocampus; increased dynorphin mRNA in the nucleus accumbens; increased GAD65 mRNA in the anterior hypothalamus and bed nucleus of the stria terminalis; and decreased GAD65 mRNA in the dorsal hypothalamus. Importantly, palatable food intake prevented stress-induced gene expression changes in subregions of the hypothalamus, bed nucleus of the stria terminalis, and nucleus accumbens. Overall, these data suggest that complex interactions exist between brain reward and stress pathways and that palatable snacking can mitigate many of the neurochemical alterations induced by chronic stress.
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影响因子：
2.9
作者：
Bruchas MR;Land BB;Chavkin C
通讯作者：
Chavkin C
影响因子：
4.1
作者：
HERMAN, JP;ADAMS, D;PREWITT, C
通讯作者：
PREWITT, C
DOI：
10.1016/0169-328x(92)90201-l
发表时间：
1992-11-01
期刊：
MOLECULAR BRAIN RESEARCH
影响因子：
--
作者：
AHIMA, RS;GARCIA, MM;HARLAN, RE
通讯作者：
HARLAN, RE
影响因子：
4.7
作者：
Dumont, EC;Kinkead, R;Drolet, G
通讯作者：
Drolet, G
影响因子：
4.7
作者：
Ikemoto, S;Wise, RA
通讯作者：
Wise, RA