ICV NPY Y1 receptor agonist but not Y5 agonist induces torpor-like hypothermia in cold-acclimated Siberian hamsters.

ICV NPY Y1 receptor agonist but not Y5 agonist induces torpor-like hypothermia in cold-acclimated Siberian hamsters.
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ICV NPY Y1 受体激动剂而非 Y5 激动剂会在冷适应的西伯利亚仓鼠中诱导类似冬眠的低温。

DOI:
10.1152/ajpregu.00790.2006
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发表时间:
2007
期刊:
American journal of physiology. Regulatory, integrative and comparative physiology
影响因子:
--
通讯作者:
Dark,John
Dark,John
中科院分区:
--
文献类型:
--
作者:
Pelz,KimberlyM;Dark,John

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由于日常生活中的麻木,导致新陈代谢减少,这使得许多小型哺乳动物,包括西伯利亚仓鼠,能够在充满活力的挑战中生存下来。很少有人知道的神经机制的启动和表现的迟钝。下丘脑神经肽Y(NPY)通过增加食物摄入和减少代谢消耗来帮助应对能量挑战。在冷驯化的西伯利亚仓鼠脑室内注射神经肽Y诱导类似于自然麻木的低温。目前已鉴定出多种NPY受体亚型,其中Y1受体和Y 5受体均参与了NPY的增食欲作用。本研究的目的是比较和对比Y1受体激动剂([d-Arg 25]-NPY)激活Y1受体和Y 5受体激动剂([d-Trp 34]-NPY)激活Y 5受体对冷驯化西伯利亚仓鼠体温和随后摄食量的影响。侧脑室注射Y1激动剂产生类似于侧脑室注射NPY引起的torporlike低温。脑室内Y 5激动剂很少产生低温,达到麻木的标准,并未能类似于NPY诱导或自然麻木。Y1和Y 5激动剂的联合注射导致与单独的Y 5激动剂治疗相当的体温降低,否定了单独的Y1激动剂所观察到的NPY治疗的模拟。Y1激动剂和Y 5激动剂对NPY诱导的沉默表达有延迟作用,Y1激动剂增强,Y 5激动剂抑制NPY的作用。NPY诱导torporlike体温过低的能力,尤其是其启动的能力,很可能涉及NPY Y1受体亚型的激活。
The reduced metabolism derived from daily torpor enables numerous small mammals, including Siberian hamsters, to survive periods of energetic challenge. Little is known of the neural mechanisms underlying the initiation and expression of torpor. Hypothalamic neuropeptide Y (NPY) contributes to surviving energetic challenges by both increasing food ingestion and reducing metabolic expenditure. Intracerebroventricular injections of NPY in cold-acclimated Siberian hamsters induce torpor-like hypothermia comparable to natural torpor. Multiple NPY receptor subtypes have been identified, and the Y1 receptor and Y5 receptor both contribute to the orexigenic effect of NPY. The purpose of this research was to compare and contrast the effects of Y1 receptor activation by a specific Y1 agonist ([d-Arg 25]-NPY) or Y5 receptor activation by a specific Y5 agonist ([d-Trp 34]-NPY) on body temperature and subsequent food intake in cold-acclimated Siberian hamsters. Intracerebroventricular injections of Y1 agonist produced torporlike hypothermia closely resembling that induced by intracerebroventricular NPY. The intracerebroventricular Y5 agonist infrequently produced hypothermia reaching criterion for torpor and that failed to resemble either NPY-induced or natural torpor. Combined injections of Y1 and Y5 agonists resulted in hypothermia comparable to Y5 agonist treatments alone, negating the mimicry of NPY treatment seen with Y1 agonist alone. Prior treatment with Y1 agonist or Y5 agonist surprisingly had lingering effects on NPY-induced torpor expression, Y1 agonist enhanced and Y5 agonist inhibited the effect of NPY. The ability of NPY to induce torporlike hypothermia, especially its initiation, most likely involves activation of the NPY Y1 receptor subtype.
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