Npy2r (mouse)
- Known as:
- Npy2r (mouse)
- Catalog number:
- Y213636
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Npy2r (mouse)
Related genes to: Npy2r (mouse)
- Gene:
- NPY2R NIH gene
- Name:
- neuropeptide Y receptor Y2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 4q32.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-10-18
- Date modifiied:
- 2015-08-25
Related products to: Npy2r (mouse)
Related articles to: Npy2r (mouse)
- Maternal aggression enables lactating females to protect their vulnerable young, yet its rapid emergence after birth and swift decline when pups are absent remain poorly understood. Our study reveals the critical role of the pathway from posterior amygdala cells expressing oestrogen receptor alpha (PA) to the ventrolateral part of ventromedial hypothalamus cells expressing neuropeptide Y receptor 2 (VMHvl) in the rise and fall of maternal aggression. Projection-specific manipulations and recordings show that PA cells projecting to the VMHvl are naturally active during attack and are required for maternal aggression. During lactation, PA-to-VMHvl synapses potentiate and VMHvl cell excitability increases, enabling heightened aggression. PA neurons express abundant oxytocin receptors, allowing oxytocin to boost PA output; after pup removal, declining oxytocin levels reduce PA drive and dampen maternal aggression, a deficit restored by pup reunion or optogenetic elevation of oxytocin. These findings reveal multiple forms of plasticity in a defined PA-VMHvl circuit that collectively implement the adaptive, need-based control of maternal aggression. - Source: PubMed
Publication date: 2026/04/15
Yamaguchi TakashiYan RongzhenKhan MashrurKuno SotaTewatia KanishkOsakada TakuyaParthasarathy SrinivasPacold Michael EShah Nirao MLin Dayu - Engrams are formed by activity-dependent recruitment of subsets of excitatory principal neurons, whereas inhibitory neurons mediate memory lability and stability. It remains elusive whether specific types of interneurons are preferentially engaged in determining the fate of memory. Here we show, in male mice undergoing cued fear memory training and extinction, that neuropeptide Y (NPY)-expressing (NPY) GABA-ergic interneurons in ventral CA1 (vCA1) exert both fast GABA-ergic inhibition to facilitate memory acquisition and slow NPY-mediated inhibition to facilitate extinction. Specifically, the calcium dynamics of NPY neurons and NPY release in vCA1 ramp up as extinction learning progresses and the behavioral state switches from 'fear-on' to 'fear-off'. We show that NPY is necessary and sufficient to control the rate and degree of memory extinction by acting on two nonoverlapping subensembles composed of NPY receptor 1 (NPY1R)-expressing and NPY2R-expressing neurons, thereby gating early fast and late slow stages of extinction, respectively. Thus, subtype-specific, slow peptidergic inhibition from interneurons regulates engram lability versus stability. - Source: PubMed
Publication date: 2026/03/31
Wu Yan-JiaoGu XueKong YaleiYang ShuoWang HuanXu MiaoWang QiYi XinLin Ze-JieJiao Zhi-HanCheung HoiyinZhao Xin-YuBian XinJiang QinLi YingZhu Michael XWang Lu-YangLi YulongHuang JuLi QianLi Wei-GuangXu Tian-Le - Neuropeptide Y (NPY) is a key regulator of energy homeostasis, acting through various receptor subtypes in both central and peripheral systems. Increasing interest has been directed toward exploiting NPY as a pharmacological target in obesity. While the orexigenic role of NPY in the hypothalamus is well established, its downstream effects on peripheral metabolism remain less defined, particularly when perturbations to the system are introduced. Previously, we observed that female mice with limbic NPY-Y1 receptor gene (Npy1r) knockout (KO) under different dietary conditions (standard, SD, or high-fat diet, HFD) accumulated more subcutaneous white adipose tissue (WAT) compared to wild-type in the absence of gonadal hormones, despite no changes in food intake. To deepen the mechanisms underlying these effects, we conducted molecular analyses on WAT of these mice. We found that Npy gene expression was upregulated in WAT of HFD-fed mice, regardless of genotype. However, NPY peptide levels were reduced in both KO and HFD groups, suggesting post-transcriptional regulation of NPY under metabolic stress. NPY-Y2 receptor gene (Npy2r) expression in WAT was significantly increased in both KO and HFD while Npy1r expression in WAT remained unchanged across groups. Genes involved in WAT metabolism were similarly upregulated in both KO and HFD mice, indicating that limbic Npy1r KO mimics some of the metabolic effects induced by HFD. Correlation analysis suggests that dysregulated NPY signalling may promote increased lipid storage and reduce energy expenditure. Overall, these findings highlight the complex interplay between central and peripheral NPY signalling emphasizing the importance of caution when investigating therapeutic strategies targeting single NPY receptors. Overall, these findings highlight the complex interplay between central Npy1r signalling and peripheral adipose tissue regulation. They also emphasize the importance of caution when investigating new therapeutic strategies targeting single NPY receptors, as central interventions may provoke maladaptive metabolic responses in peripheral tissues. - Source: PubMed
Publication date: 2026/03/20
Einaudi GiacomoOberto AlessandraBertocchi IlariaAimaretti EleonoraFerreira Alves GustavoPorchietto ElisaCifani CarloMicioni Di Bonaventura Maria VittoriaCollino MassimoChiazza Fausto - Numerous peptide hormones regulate feeding and metabolism via the brain and alimentary canal. Many of these peptides are also expressed, along with their cognate receptors, in the taste buds of the lingual epithelium. Among those present in the rodent oral cavity are peptides and receptors in the neuropeptide Y (NPY) family. Previous studies suggest that manipulation of NPY family peptide signaling can impact upon taste-related behavior, but it remains unclear whether these are mediated by changes in taste information processed by taste bud cells (TBCs), the primary sensory organs of the gustatory system, and whether human taste buds are similarly impacted by NPY family peptide signaling. In this report, we identify a complex modulatory role for NPY family peptides in shaping the tastant-evoked responses of human TBCs. Using a human fungiform taste bud cell line, we show that NPY and peptide YY (PYY), along with NPY receptor subtypes 1 and 2 (NPY1R and NPY2R), are expressed in TBCs. Importantly, NPY and PYY modulated the functional responses (assessed by calcium imaging and measurements of neurotransmitter release) of TBCs to bitter and fatty acid stimuli. The nature of modulation (i.e., enhancement or diminishment) was dependent not only on the peptide but also on the taste modality in question. Application of NPY1R and NPY2R antagonists indicated that the differential impacts of these peptides on TBC response parameters were mediated by differential NPY receptor activation. These data suggest that NPY family peptides directly and intricately modify gustatory sensory input by shaping TBC signaling. The conventional view of feeding regulation by metabolic peptides largely comprises "top-down" peptidergic signaling via the hypothalamus incorporating pre- and postprandial information via the gut-brain axis. Here, we suggest a role for these peptides adjusting "bottom-up" taste information streams that impact food choice and intake. This novel dimension of peptidergic modulation may provide a more comprehensive understanding of taste, feeding, and metabolism that better informs diagnostic and therapeutic developments related to feeding and metabolic regulation. - Source: PubMed
Publication date: 2026/03/11
Iyer SatyaGangakhedkar RitikaBhuiyan IreneMontmayeur Jean-PierreDotson Cedrick D - The genetic architecture of Parkinson's disease (PD) and progression to PD dementia (PDD) remains incompletely characterized in Asians. Here, we investigated genetic risk factors for PD and PDD in Taiwanese individuals from the Taiwan Precision Medicine Initiative (TPMI), the largest non-European cohort integrating genetic and electronic medical record data. - Source: PubMed
Publication date: 2026/03/04
Lin Chin-HsienChang Chien-ChingChen Hung-HsinLin Wan-JiaHsu Chia-LangLin Rung-JuenGuo Yi-JenFang Ting-ChunLin Shinn-ZongHuang Chih-YangWang Shuu-JiunHang Jen-FanHsieh Sun-WungChou Mei-ChuanYeh Tu-HsuehHu Chaur-JongYang Fu-ChiChang Hsin-AnLee Tsong-HaiTsai Meng-HanKuo Ming-CheLiou Jyh-MingWu Ming-ShiangPark Kye WonChung Sun JuTan Eng-KingShen-Jang Fann Cathy