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首页> 外文期刊>American Journal of Physiology >Intermittent access to sucrose increases sucrose-licking activity and attenuates restraint stress-induced activation of the lateral septum
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Intermittent access to sucrose increases sucrose-licking activity and attenuates restraint stress-induced activation of the lateral septum

机译:间歇性获取蔗糖可增加蔗糖舔活性,并减弱束缚应激诱导的外侧隔的激活

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Intermittent access to palatable food can attenuate anorectic and hormonal responses to stress in rats. The neuronal mechanisms of modulation of stress response by diets are not fully understood. The present study was conducted to create rat models with intermittent access to sucrose that demonstrate resistance to stress-induced hypophagia, to study the pattern of sucrose consumption by these rat models, and to investigate in which brain structures intermittent sucrose regimens modify stressinduced neuronal activation. The obtained results demonstrate that 6-wk intermittent access to sucrose without food restriction (4 day/wk ad libitum access to sucrose in addition to chow, and following 3 day/wk exclusive feeding of chow; SIA rats) and combined with food restriction (4 day/wk access to chow and sucrose restricted to 2 h/day, and following 3 days/wk on unrestricted chow; SIR rats) increased sucrose-licking activity. The alterations in the rats' feeding behavior were accompanied by a resistance of their body weight gain and food intake to 1-h restraint stress applied once per week. The chronic intermittent sucrose consumption significantly lowered, in the SIA and SIR rats, the levels of expression of corticotropin-releasing factor type 2 receptor and restraint stress-induced expression of c-fos mRNA in the medioventral part of the lateral septum. Conversely, the levels of the corticotropin-releasing factor type 2 receptor transcript in the ventromedial hypothalamic nucleus were decreased only in the foodrestricted SIR rats. The lower stress-induced neuronal activation in the medioventral part of the lateral septum may contribute to the attenuated anorectic stress response in the rats maintained on intermittent sucrose regimens.
机译:间歇性获得可口食物可以减弱大鼠对压力的厌食和激素反应。饮食对应激反应调节的神经机制尚不完全清楚。进行本研究的目的是创建可间歇性访问蔗糖的大鼠模型,该模型显示出对应激诱导的吞咽能力的抵抗力,以研究这些大鼠模型消耗蔗糖的模式,并研究间歇性蔗糖治疗方案在哪些脑结构中修饰应激诱导的神经元活化。获得的结果表明,在没有食物限制的情况下可以连续6周间歇地获取蔗糖(除了食物之外,还可以自由获取4周/周的蔗糖,并且在3周/周之后才单独充入食物; SIA大鼠)并与食物限制相结合(每周4天/周的食物和蔗糖限制为2小时/天,而之后3天/周的不受限制的食物; SIR大鼠)增加了舔蔗糖的活性。大鼠摄食行为的改变伴随着它们的体重增加和食物摄入对每周施加1小时的约束压力的抵抗。在SIA和SIR大鼠中,慢性间歇性蔗糖消耗显着降低了侧隔中隔腹部分中促肾上腺皮质激素释放因子2型受体的表达水平和抑制应激诱导的c-fos mRNA表达。相反,腹膜下丘脑核中促肾上腺皮质激素释放因子2型受体转录物的水平仅在受食物限制的SIR大鼠中降低。侧隔中腹内侧较低的应激诱导的神经元激活可能有助于维持间歇性蔗糖治疗的大鼠的厌食应激反应减弱。

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