GENETICS OF NEUROPEPTIDE Y FUNCTION
神经肽 Y 功能的遗传学
基本信息
- 批准号:6160020
- 负责人:
- 金额:$ 14.83万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2000
- 资助国家:美国
- 起止时间:2000-08-01 至 2002-07-31
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
DESCRIPTION (applicant's abstract): Neuropeptide Y (NPY) has been implicated in
the regulation of appetite and energy balance because (a) centrally
administered NPY stimulates robust feeding, (b) NPY mRNA and protein levels
rise in the arcuate nucleus of the hypothalamus under conditions of reduced
energy balance, as well as in ob/ob mice that lack leptin and consequently
become hyperphagic. Moreover, intervention of NPY signaling by administering
anti-sense oligonucleotides, antibodies or NPY receptor antagonists generally
inhibits feeding. Thus, it was a surprise that knock-out mice unable to make
NPY had normal body weight regulation. The genetic results clearly indicate
that NPY is not essential for feeding under the conditions examined, but they
do not address the question of whether NPY is acutely involved in regulation of
appetite. It is possible that chronic absence of NPY triggers compensatory
mechanisms. This proposal aims to use genetic techniques to explore several
potential forms of compensation. The specific aims address the following
questions: (1) Does agouti related protein (AgRP) compensate for NPY
deficiency?, (2) Do the neurons that make NPY and AgRP in the arcuate nucleus
produce other neuromodulators that may compensate for NPY deficiency?, and (3)
Does acute inactivation of NPY gene expression in the adult affect appetite and
energy balance? The first aim will be addressed by generating mice in which
both NPY and AgRP genes are inactivated. If AgRP compensates for NPY, then
these mice should be lean. The second aim relies on genetic ablation of the
neurons that make NPY and AgRP. If those neurons are important for energy
balance, then those mice should be lean. The last aim is addressed by creating
mice with a NPY gene that can be inactivated at will. Inactivation of NPY
expression in the adult may have transient or chronic effects on regulation of
appetite and energy balance. These genetic experiments should help rationalize
the current disparate results obtained by permanent NPY gene silencing and by
acute intervention of NPY signaling.
描述(申请人摘要):神经肽Y(NPY)与
食欲和能量平衡的调节,因为(a)中央
施用的NPY刺激健壮的进食,(B)NPY mRNA和蛋白质水平
下丘脑弓状核的上升,
能量平衡,以及缺乏瘦素的ob/ob小鼠,
变得贪食此外,通过给予
反义寡核苷酸、抗体或NPY受体拮抗剂通常
抑制进食。因此,令人惊讶的是,敲除小鼠不能使
NPY具有正常的体重调节功能。基因检测结果清楚地表明
NPY在所检查的条件下对于进食不是必需的,但它们
没有解决NPY是否严重参与调节的问题,
胃口这可能是因为长期缺乏神经肽Y触发了代偿性
机制等这项建议旨在利用遗传技术探索几个
可能的补偿方式。具体目标如下
问题:(1)AgRP是否补偿NPY
缺陷?(2)弓状核内产生NPY和AgRP的神经元
产生其他的神经调质来补偿神经肽Y的缺乏?以及(3)
成人NPY基因表达的急性失活是否影响食欲和
能量平衡?第一个目标将通过产生小鼠来实现,
NPY和AgRP基因都失活。如果AgRP补偿了NPY,那么
这些老鼠应该很瘦第二个目标依赖于基因消融,
产生NPY和AgRP的神经元。如果这些神经元对能量很重要
平衡,那么这些老鼠应该是瘦的。最后一个目标是通过创建
一种可以随意失活的神经肽Y基因小鼠。NPY失活
在成人中的表达可能对调节
食欲和能量平衡。这些基因实验应该有助于合理化
目前,通过永久性NPY基因沉默和
NPY信号的急性干预。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Richard D. Palmiter其他文献
Purification and translation of ovalbumin, conalbumin, ovomucoid and lysozyme messenger RNA
- DOI:
10.1007/bf00357152 - 发表时间:
1973-10-01 - 期刊:
- 影响因子:2.800
- 作者:
Richard D. Palmiter;Lynne T. Smith - 通讯作者:
Lynne T. Smith
Hormonal induction and regulation of lactose synthetase in mouse mammary gland.
小鼠乳腺中乳糖合成酶的激素诱导和调节。
- DOI:
10.1042/bj1130409 - 发表时间:
1969 - 期刊:
- 影响因子:0
- 作者:
Richard D. Palmiter - 通讯作者:
Richard D. Palmiter
Parabrachial neurons promote nociplastic pain
臂旁神经元会加剧神经塑性疼痛
- DOI:
10.1016/j.tins.2024.07.002 - 发表时间:
2024-09-01 - 期刊:
- 影响因子:15.100
- 作者:
Richard D. Palmiter - 通讯作者:
Richard D. Palmiter
Parabrachial <em>Calca</em> neurons drive nociplasticity
- DOI:
10.1016/j.celrep.2024.114057 - 发表时间:
2024-04-23 - 期刊:
- 影响因子:
- 作者:
Logan F. Condon;Ying Yu;Sekun Park;Feng Cao;Jordan L. Pauli;Tyler S. Nelson;Richard D. Palmiter - 通讯作者:
Richard D. Palmiter
Edinger-Westphal Urocortin-1 neurons regulate consumption and affect
埃丁格-韦斯特法尔促肾上腺皮质激素释放因子相关肽-1神经元调节消耗量并产生影响
- DOI:
10.1016/j.celrep.2025.115814 - 发表时间:
2025-06-24 - 期刊:
- 影响因子:6.900
- 作者:
Rebecca J. Bluett;Ying Yu;Jordan L. Pauli;Carlos A. Campos;Richard D. Palmiter - 通讯作者:
Richard D. Palmiter
Richard D. Palmiter的其他文献
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{{ truncateString('Richard D. Palmiter', 18)}}的其他基金
Effect of killing or removing GABA from NPY/AgRP neurons
杀死或去除 NPY/AgRP 神经元中 GABA 的作用
- 批准号:
8290732 - 财政年份:2007
- 资助金额:
$ 14.83万 - 项目类别:
Effect of Killing or Removing GABA from NPY/AgRP Neurons
杀死或去除 NPY/AgRP 神经元中 GABA 的效果
- 批准号:
7196113 - 财政年份:2007
- 资助金额:
$ 14.83万 - 项目类别:
Effect of killing or removing GABA from NPY/AgRP neurons
杀死或去除 NPY/AgRP 神经元中 GABA 的作用
- 批准号:
8446978 - 财政年份:2007
- 资助金额:
$ 14.83万 - 项目类别:
Effect of Killing or Removing GABA from NPY/AgRP Neurons
杀死或去除 NPY/AgRP 神经元中 GABA 的效果
- 批准号:
7652490 - 财政年份:2007
- 资助金额:
$ 14.83万 - 项目类别:
Effect of Killing or Removing GABA from NPY/AgRP Neurons
杀死或去除 NPY/AgRP 神经元中 GABA 的效果
- 批准号:
7501294 - 财政年份:2007
- 资助金额:
$ 14.83万 - 项目类别:
Effect of Killing or Removing GABA from NPY/AgRP Neurons
杀死或去除 NPY/AgRP 神经元中 GABA 的效果
- 批准号:
7880182 - 财政年份:2007
- 资助金额:
$ 14.83万 - 项目类别:
Effect of killing or removing GABA from NPY/AgRP neurons
杀死或去除 NPY/AgRP 神经元中 GABA 的作用
- 批准号:
9043003 - 财政年份:2007
- 资助金额:
$ 14.83万 - 项目类别:
Effect of killing or removing GABA from NPY/AgRP neurons
杀死或去除 NPY/AgRP 神经元中 GABA 的作用
- 批准号:
8636000 - 财政年份:2007
- 资助金额:
$ 14.83万 - 项目类别:
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