Characterization and presynaptic modulation of stimulation-evoked exocytotic co-release of noradrenaline and neuropeptide Y in guinea pig heart
90
Citation
47
Reference
10
Related Paper
Citation Trend
The neuropeptide BW receptor 1 (NPBW1, provisional nomenclature [6]) is activated by two 23-amino-acid peptides, neuropeptide W (neuropeptide W-23) and neuropeptide B (neuropeptide B-23) [22, 7]. C-terminally extended forms of the peptides (neuropeptide W-30 and neuropeptide B-29) also activate NPBW1 [2]. Unique to both forms of neuropeptide B is the N-terminal bromination of the first tryptophan residue, and it is from this post-translational modification that the nomenclature NPB is derived. These peptides were first identified from bovine hypothalamus and therefore are classed as neuropeptides. Endogenous variants of the peptides without the N-terminal bromination, des-Br-neuropeptide B-23 and des-Br-neuropeptide B-29, were not found to be major components of bovine hypothalamic tissue extracts. The NPBW2 receptor is activated by the short and C-terminal extended forms of neuropeptide W and neuropeptide B [2].
Cite
Citations (0)
Cite
Citations (25)
Basal (medicine)
Cite
Citations (124)
Since the discovery of neuropeptide Y which is co‐stored and co‐operate with noradrenaline (NA) in sympathetic nerve fibers, several scientific groups have searched for structures with neuropeptide Y antagonistic properties. Research has mainly focused on various peptide fragments which originate from or are related to the neuropeptide Y sequence. Some non‐peptide antagonists have been proposed but they are mostly of low potency and non‐selective. Our recent observations that α‐trinositol (D‐myo‐inositol 1.2.6‐trisphosphate) is an inhibitor of neuropeptide Y effects will hopefully lead to the development of useful non‐peptide neuropeptide Y inhibitors. As a novel approach the highly selective approach of down‐regulating neuropeptide Y receptors with antisense oligodeoxynucleotides is also discussed. Neuropeptide Y antagonistic agents would help us to understand the physiological role of neuropeptide Y and may serve as useful medication in circulation disorders.
Cite
Citations (22)
Neuropeptide Y (NPY ) 是为喂的有势力 neurotransmitter。也除 NPY，象刺鼠相关的蛋白质(AgRP ) 那样的开胃 neuropeptides，和象刺激荷尔蒙(MSH ) 和 cocaine-amphetamine-regulated 抄本(大车) 的 alpha-melatonin 那样的使食欲不振 neuropeptides 以外涉及中央喂规定。在禁食期间， NPY 和 AgRP 基因表情是起来调整的， POMC 和大车基因表情在视下丘是下面调整的。基于 peptidergic 神经原的网络，前者涉及积极的喂规定，和后者涉及否定的喂，它特别在帕拉施加这些喂养, 饲, 哺调整肽室的原子核(PVN ) 。在喂上澄清 NPY 系统的大美人的补偿机制，在胃口相关的 neuropeptides 和喂的行为的基因表情的变化在 NPY Y5 击倒老鼠被学习。食物摄取在 Y5 击倒老鼠被增加。禁食更深刻地在 KO 老鼠增加了食物和水吸入的数量。这些数据显示了在 Y5 击倒鼠标喂行为的补偿现象。RT-PCR 和 ISH 建议喂的赔偿在视下丘由于在 AgRP，大车和 POMC 的基因表情的变化。因此，这些调查结果显示补偿机制在弓形的原子核(弧) 在 POMC/CART 基因表示包含变化。POMC/CART 基因表示为在喂行为的中央补偿规定是重要的。
Cart
Cite
Citations (0)
Pancreatic polypeptide
Peptide YY
Cite
Citations (60)
Elevated levels of immunoreactive hypothalamic neuropeptide Y have recently been reported both in streptozotocin‐induced diabetic rats and in the spontaneously diabetic BB rat. We have measured the levels of neuropeptide Y encoding messenger ribonucleic acid (mRNA) in both of these rat models to determine whether an increase in neuropeptide Y gene expression is a contributory factor to the increases in hypothalamic neuropeptide Y immunoreactive peptide content. In the hypothalami of both the spontaneously diabetic BB/E and the streptozotocin‐diabetic animals, neuropeptide Y mRNA showed significant elevations (to 204 ± 13% (± SE) and 387 ± 48% of control values, respectively, p < 0.01 for both). Our results demonstrate that two models of insulin‐deficient diabetes in the rat are associated with increased hypothalamic neuropeptide Y mRNA. Taken with the known effects of neuropeptide Y on food intake these results suggest that increased neuropeptide Y synthesis in the hypothalamus may be related to the hyperphagia seen in the diabetic condition.
Cite
Citations (22)
Cite
Citations (33)
Peptide YY
Orexigenic
Radioligand
Cite
Citations (11)