Neuropeptides最新文献_第8页

Neuropeptide Y Y2 receptors in acute and chronic pain and itch 神经肽 Y Y2 受体在急性和慢性疼痛和瘙痒中的作用。

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-12-01 Epub Date: 2024-10-18 DOI: 10.1016/j.npep.2024.102478

Paramita Basu , Bradley K. Taylor

{"title":"Neuropeptide Y Y2 receptors in acute and chronic pain and itch","authors":"Paramita Basu , Bradley K. Taylor","doi":"10.1016/j.npep.2024.102478","DOIUrl":"10.1016/j.npep.2024.102478","url":null,"abstract":"<div><div>Pain and itch are regulated by a diverse array of neuropeptides and their receptors in superficial laminae of the spinal cord dorsal horn (DH). Neuropeptide Y (NPY) is normally expressed on DH neurons but not sensory neurons. By contrast, the Npy2r receptor (Y2) is expressed on the central and peripheral terminals of sensory neurons but not on DH neurons. Neurophysiological slice recordings indicate that Y2-selective agonists inhibits spinal neurotransmitter release from sensory neurons. However, behavioral pharmacology studies indicate that Y2 agonists exert minimal changes in nociception, even after injury. Additional discrepancies in the behavioral actions of the Y2-antagonist BIIE0246 – reports of either pronociception or antinociception – have now been resolved. In the normal state, spinally-directed (intrathecal) administration of BIIE0246 elicits ongoing nociception, hypersensitivity to sensory stimulation, and aversion. Conversely, in the setting of nerve injury and inflammation, intrathecal BIIE024 reduced not only mechanical and thermal hypersensitivity, but also a measure of the affective dimension of pain (conditioned place preference). When administered in chronic pain models of latent sensitization, BIIE0246 produced a profound reinstatement of pain-like behaviors. We propose that tissue or nerve injury induces a G protein switch in the action of NPY-Y2 signaling from antinociception in the naïve state to the inhibition of mechanical and heat hyperalgesia in the injured state, and then a switch back to antinociception to keep LS in a state of remission. This model clarifies the pharmacotherapeutic potential of Y2 research, pointing to the development of a new non-opioid pharmacotherapy for chronic pain using Y2 antagonists in patients who do not develop LS.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102478"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

GnRH protective effects against long-term potentiation impairment induced by AANAT-siRNA GnRH对AANAT-siRNA诱导的长期延时损伤的保护作用

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-12-01 Epub Date: 2024-09-18 DOI: 10.1016/j.npep.2024.102474

Leila Karimi-Zandi , Tahereh Ghorbandaiepour , Maryam Zahmatkesh , Esmaeil Sadroddiny

{"title":"GnRH protective effects against long-term potentiation impairment induced by AANAT-siRNA","authors":"Leila Karimi-Zandi , Tahereh Ghorbandaiepour , Maryam Zahmatkesh , Esmaeil Sadroddiny","doi":"10.1016/j.npep.2024.102474","DOIUrl":"10.1016/j.npep.2024.102474","url":null,"abstract":"<div><div>There is an interplay between the gonadotropin-releasing hormone (GnRH) and melatoninergic systems. The key enzyme of melatonin synthesis (arylalkylamine <em>N</em>-acetyltransferase, AANAT), and GnRH receptors are expressed in the hippocampus. While it has been shown that hippocampal AANAT enzyme activity is necessary for proper hippocampal cognitive function, their role in long-term potentiation (LTP) induction is not fully understood. In current study, the impact of GnRH on LTP induction was investigated, while hippocampal melatonin synthesis had been inhibited. The melatonin synthesis was inhibited by AANAT-siRNA administration, and LTP was induced using in vivo field potential electrophysiological recording.</div><div>Animals were divided into 5 groups: Intact, vehicle, siRNA, GnRH and siRNA+GnRH. All animals, except intact group, experienced the stereotaxic surgery and intra-hippocampal cannulation to receive vehicle agent, AANAT siRNA (0.5 μg/hip), GnRH (1 ng/rat), and AANAT siRNA+GnRH. The recognition memory was assessed by Novel object recognition test. The field potential electrophysiology experiment was conducted by stimulating the Schaffer collateral pathway, and LTP induction was carried out through high-frequency stimulation (HFS). After recording, animals' brain was isolated and quickly frozen for further hippocampal melatonin levels measurement by LC-MS and AANAT mRNA levels by qRT-PCR.</div><div>GnRH injection in the hippocampus increased local AANAT-mRNA expression and melatonin levels. GnRH-treated animals displayed higher LTP amplitude compared to intact, vehicle and siRNA groups. While the reduction in hippocampal melatonin levels by AANAT-siRNA inhibited LTP and impaired recognition memory, the GnRH prevented these adverse effects. The data suggests that GnRH have protective effects against AANAT-siRNA-induced LTP decline. The protective mechanism at least partially, may be related to the increased expression of local AANAT-mRNA.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102474"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142292235","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enteroendocrine cell-derived peptide YY signalling is stimulated by pinolenic acid or Intralipid and involves coactivation of fatty acid receptors FFA1, FFA4 and GPR119 蒎烯酸或 Intralipid 可刺激肠内分泌细胞衍生的肽 YY 信号，并涉及脂肪酸受体 FFA1、FFA4 和 GPR119 的协同激活。

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-12-01 Epub Date: 2024-10-11 DOI: 10.1016/j.npep.2024.102477

Iain R. Tough, Runisha Moodaley, Helen M. Cox

{"title":"Enteroendocrine cell-derived peptide YY signalling is stimulated by pinolenic acid or Intralipid and involves coactivation of fatty acid receptors FFA1, FFA4 and GPR119","authors":"Iain R. Tough, Runisha Moodaley, Helen M. Cox","doi":"10.1016/j.npep.2024.102477","DOIUrl":"10.1016/j.npep.2024.102477","url":null,"abstract":"<div><div>Long chain fatty acids are sensed by enteroendocrine L cells that express free-fatty acid receptors, including FFA1, FFA4 and the acylethanolamine receptor GPR119. Here we investigated the acute effects of single or multiple agonism at these G protein-coupled receptors in intestinal mucosae where L cell-derived peptide YY (PYY) is anti-secretory and acts via epithelial Y<sub>1</sub> receptors. Mouse ileal or colonic mucosae were mounted in Ussing chambers, voltage-clamped and the resultant short-circuit current (I<sub>sc</sub>) recorded continuously. The agonists used were; FFA1, TAK-875 or AM-1638; for FFA4, Merck A; or for GPR119, AR231453, PSN632408 or AR440006. Their responses were compared with those of pinolenic acid (PA, a presumed dual FFA1/FFA4 agonist) and the lipid emulsion, Intralipid. The FFA1 agonist AM-1638 (EC<sub>50</sub> = 38.2 nM) was more potent than TAK-875 (EC<sub>50</sub> = 203.1 nM) but exhibited similar efficacy. GPR119 agonism (AR231453) pretreatment enhanced subsequent FFA1 (AM-1638 or TAK-875) and FFA4 (Merck A) signalling. PA (EC<sub>50</sub> = 298.2 nM) co-activated epithelial FFA1 and FFA4 and involved endogenous PYY Y<sub>1</sub>/Y<sub>2</sub>-receptor mechanisms but desensitisation was observed between PA and high GPR119 agonist concentrations. Apical Intralipid co-activated FFA1, FFA4 and GPR119 with a residual component not being attributable to PYY, or this trio of fatty acid receptors.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"108 ","pages":"Article 102477"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142471043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The activity of cholinergic neurons in the basal forebrain interferes with anesthesia-arousal process of propofol 前脑基底胆碱能神经元的活动干扰异丙酚的麻醉-唤醒过程

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-10-01 Epub Date: 2024-06-14 DOI: 10.1016/j.npep.2024.102449

Cai-hua Feng , Xiao-Nan Du , Zhi Wang , Ting Wu , Li-Na Zhang

{"title":"The activity of cholinergic neurons in the basal forebrain interferes with anesthesia-arousal process of propofol","authors":"Cai-hua Feng , Xiao-Nan Du , Zhi Wang , Ting Wu , Li-Na Zhang","doi":"10.1016/j.npep.2024.102449","DOIUrl":"10.1016/j.npep.2024.102449","url":null,"abstract":"<div><p>Previous research has demonstrated that basal forebrain (BF) regulates arousal during propofol anesthesia. However, as the BF comprises cholinergic neurons alongside two other types of neurons, the specific role of cholinergic neurons has not been definitively elucidated. In our study, calcium signal imaging was utilized to monitor the real-time activities of cholinergic neurons in the BF during propofol anesthesia. Additionally, we selectively stimulated these neurons to investigate EEG and behavioral responses during propofol anesthesia. Furthermore, we specifically lesioned cholinergic neurons in the BF to investigate the sensitivity to propofol and the induction time. The results revealed that propofol suppressed calcium signals of cholinergic neurons within the BF following intraperitoneal injection. Notably, upon recovery of the righting reflex, the calcium signals partially recovered. Spectral analysis of the EEG elucidated that optical stimulation of cholinergic neurons led to a decrease in δ power underlie propofol anesthesia. Conversely, depletion of cholinergic neurons in the BF enhanced sensitivity to propofol and shortened the induction time. These findings clarify the role of cholinergic neurons in the anesthesia-arousal process, as well as the depth and the sensitivity of propofol anesthesia.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102449"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0143417924000489/pdfft?md5=2954f2a19297b9c76679046ebce2f747&pid=1-s2.0-S0143417924000489-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141409489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The restraint stress-induced antinociceptive effects decreased by antagonism of both orexin receptors within the CA1 region of the hippocampus 拮抗海马 CA1 区的两种奥曲肽受体可降低束缚应激引起的抗痛觉效应

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-10-01 Epub Date: 2024-08-22 DOI: 10.1016/j.npep.2024.102463

Elaheh Danesh , Shahin Hassanpour , Bita Vazir , Mohammad Saghafi , Mohadeseh Ghalandari-Shamami , Abbas Haghparast

{"title":"The restraint stress-induced antinociceptive effects decreased by antagonism of both orexin receptors within the CA1 region of the hippocampus","authors":"Elaheh Danesh , Shahin Hassanpour , Bita Vazir , Mohammad Saghafi , Mohadeseh Ghalandari-Shamami , Abbas Haghparast","doi":"10.1016/j.npep.2024.102463","DOIUrl":"10.1016/j.npep.2024.102463","url":null,"abstract":"<div><p>Studies have indicated that stress-related symptoms can lead to hormonal and neural changes, affecting the pain threshold and nociceptive behaviors. The precise role of orexin receptors (OX1r and OX2r) in stress-induced analgesia (SIA) remains an inquiry yet to be comprehensively elucidated. The current investigation aimed to assess the impact of acute immobilization restraint stress on pain-related behavioral responses after administering antagonists targeting OX1r and OX2r in a rat model using the tail-flick test. After a period of five to seven days post-stereotaxic surgery in CA1, the baseline tail-flick latency (TFL) was recorded for each animal. Subsequently, rats were unilaterally administered varying doses of the OX1r antagonist (SB334867; 1, 3, 10, and 30 nmol), the OX2r antagonist (TCS OX2 29; 1, 3, 10, and 30 nmol), or a vehicle (0.5 μl solution containing 12% DMSO) through an implanted cannula. Following a 5-min interval, the animals were subjected to a restraint stress (RS) lasting for 3 h. The tail-flick test was conducted after the stress exposure, and the TFLs were assessed at 60-min intervals. The findings of this study revealed that RS elicits antinociceptive responses in the tail-flick test. Microinjection of OX1r and OX2r antagonists into the CA1 attenuated RS-induced analgesia during the tail-flick test. Furthermore, the results underscored the preeminent role of OX2 receptors in modulating SIA. In conclusion, the orexin system localized within the hippocampal CA1 region may, in part, contribute to the manifestation of SIA in the context of acute pain.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102463"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142050135","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bezafibrate protects blood-brain barrier (BBB) integrity against traumatic brain injury mediated by AMPK 贝扎贝特能在 AMPK 的介导下保护血脑屏障（BBB）的完整性，防止脑外伤。

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-10-01 Epub Date: 2024-06-22 DOI: 10.1016/j.npep.2024.102450

Xiubao Yang, Qingyong Chang, Yan Wang, Shicang Dong, Kai Qu

{"title":"Bezafibrate protects blood-brain barrier (BBB) integrity against traumatic brain injury mediated by AMPK","authors":"Xiubao Yang, Qingyong Chang, Yan Wang, Shicang Dong, Kai Qu","doi":"10.1016/j.npep.2024.102450","DOIUrl":"10.1016/j.npep.2024.102450","url":null,"abstract":"<div><p>Bezafibrate (BEZ) has displayed a wide range of neuroprotective effects in different types of neurological diseases. However, its pharmacological function in traumatic brain injury (TBI) is still unknown. In the current study, a TBI model was constructed in mice to examine the potential beneficial roles of BEZ. After TBI, mice were daily dieted with BEZ or vehicle solution. The motor function, learning and memory, brain edema, vascular inflammatory factors, the integrity of the blood-brain barrier (BBB), and the expression of the tight junction zona occludens 1 (ZO-1) were assessed. The findings demonstrate that after TBI, BEZ treatment significantly promoted the recovery of motor function and cognitive function deficits. Moreover, BEZ attenuated brain edema by reducing the levels of brain water content. We also found that administration of BEZ alleviated cerebral vascular pro-inflammation by suppressing the expression of ICAM-1, VCAM-1, and <em>E</em>-selectin. Notably, BEZ improved the impaired BBB integrity in TBI mice by restoring the expression of the tight junction (TJ) protein ZO-1. Further in vitro experiments show that treatment with BEZ prevented the aggravation of endothelial permeability and restored the reduction of trans-epithelial electrical resistance (TEER) as well as the expression of ZO-1 in TBI-exposed brain bEnd.3 cells. Mechanistically, we prove that the protective effects of BEZ are mediated by AMPK. Based on these findings, we conclude that BEZ improves TBI-induced BBB injury and it might be considered for the treatment or management of TBI.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102450"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141603982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Biochemical characterization of Prokineticin 2 binding to Prokineticin receptor 1 in zebrafish 斑马鱼促红细胞生成素 2 与促红细胞生成素受体 1 结合的生化特征

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-10-01 Epub Date: 2024-07-25 DOI: 10.1016/j.npep.2024.102456

Roberta Lattanzi , Maria Rosaria Fullone , Alessio De Biase , Daniela Maftei , Martina Vincenzi , Rossella Miele

{"title":"Biochemical characterization of Prokineticin 2 binding to Prokineticin receptor 1 in zebrafish","authors":"Roberta Lattanzi , Maria Rosaria Fullone , Alessio De Biase , Daniela Maftei , Martina Vincenzi , Rossella Miele","doi":"10.1016/j.npep.2024.102456","DOIUrl":"10.1016/j.npep.2024.102456","url":null,"abstract":"<div><p>Prokineticin 2 (PK2) binds to prokineticin receptor 1 and prokineticin receptor 2 (PKR1 and PKR2, respectively), two G protein-coupled receptors (GPCRs) that can mediate multiple signalling pathways by promoting the elevation of intracellular calcium and cAMP levels, phosphorylation of Akt and activation of ERK and STAT3. This work aims to evidence the conservation of protein sequence and the mechanism of PK2 binding to PKR1 to use the zebrafish model for the identification of new drugs as targets of prokineticin receptors. To this end, we first demonstrated that the zebrafish genes <em>pk2</em> and <em>pkr1</em> are phylogenetically related to orthologous mammalian genes by constructing evolutionary trees and performing syntenic analyses. Subsequently, by comparing the amino acid sequences, we showed that the interaction sites with PK2 are conserved in the zPKR1. Using GST pull-down and cross-linking experiments, we demonstrated the crucial role of the N-terminal region of zPKR1 for binding to the PK2. Finally, by expressing zPKR1 in CHO cells, we demonstrated the ability of zPKR1 to induce the activation of ERK and STAT3.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102456"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141842171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Research progress on the protection and mechanism of active peptides in Alzheimer's disease and Parkinson's disease 关于阿尔茨海默病和帕金森病中活性肽的保护作用和机制的研究进展。

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-10-01 Epub Date: 2024-07-25 DOI: 10.1016/j.npep.2024.102457

Xuying Ding , Yutong Chen , Xiaojun Zhang , Yanming Duan , Guojing Yuan , Chang Liu

{"title":"Research progress on the protection and mechanism of active peptides in Alzheimer's disease and Parkinson's disease","authors":"Xuying Ding , Yutong Chen , Xiaojun Zhang , Yanming Duan , Guojing Yuan , Chang Liu","doi":"10.1016/j.npep.2024.102457","DOIUrl":"10.1016/j.npep.2024.102457","url":null,"abstract":"<div><p>Neurodegenerative diseases are the main causes of death and morbidity among elderly people worldwide. From the pathological point of view, oxidative stress, neuroinflammation, mitochondrial damage and apoptosis are the causes of neuronal diseases, and play a harmful role in the process of neuronal cell death and neurodegeneration. The most common neurodegenerative diseases are Alzheimer's disease(AD) and Parkinson's disease(PD), and there is no effective treatment. The physiological role of active peptides in the human body is significant. Modern medical research has found that animal and plant peptides, natural peptides in human body, can act on the central nervous system, and their active components can improve learning and memory ability, and play the roles of antioxidation, anti-inflammation, anti-apoptosis and maintaining the structure and function of mitochondria. This review reviews the reports on neurodegenerative diseases such as AD and PD by active peptides from animals and plants and natural peptides from the human body, and summarizes the neuroprotective mechanism of peptides. A theoretical basis for further research and development of active peptides was provided by examining the research and application of peptides, which provided a theoretical basis for further research and development.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102457"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141788742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bee venom as a promising therapeutic strategy in central nervous system diseases 蜂毒是一种治疗中枢神经系统疾病的有效方法。

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-10-01 Epub Date: 2024-06-22 DOI: 10.1016/j.npep.2024.102451

Zeinab Vahidinia , Shirin Barati , Abolfazl Azami Tameh , Saeid Bagheri-Mohammadi , Ali Garshasebi

{"title":"Bee venom as a promising therapeutic strategy in central nervous system diseases","authors":"Zeinab Vahidinia , Shirin Barati , Abolfazl Azami Tameh , Saeid Bagheri-Mohammadi , Ali Garshasebi","doi":"10.1016/j.npep.2024.102451","DOIUrl":"10.1016/j.npep.2024.102451","url":null,"abstract":"<div><p>Central nervous system (CNS) disorders are one of the leading health problems today, accounting for a large proportion of global morbidity and mortality. Most these disorders are characterized by high levels of oxidative stress and intense inflammatory responses in degenerated neuronal tissues. While extensive research has been conducted on CNS diseases, but few breakthroughs have been made in treatment methods. To date, there are no disease-modifying drugs available for CNS treatment, underscoring the urgent need for finding effective medications. Bee venom (BV), which is produced by honeybee workers' stingers, has been a subject of interest and study across various cultures. Over the past few decades, extensive research has focused on BV and its therapeutic potentials. BV consists a variety of substances, mainly proteins and peptides like melittin and phospholipase A2 (PLA2). Research has proven that BV is effective in various medical conditions, including pain, arthritis and inflammation and CNS disorders such as Multiple sclerosis, Alzheimer's disease and Parkinson's disease. This review provides a comprehensive overview of the existing knowledge concerning the therapeutic effects of BV and its primary compounds on various CNS diseases. Additionally, we aim to shed light on the potential cellular and molecular mechanisms underlying these effects.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102451"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141469713","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Chemogenetic activation ofarcuate nucleus NPY and NPY/AgRP neurons increases feeding behaviour in mice 用化学方法激活阿尔卡特核NPY和NPY/AgRP神经元可增加小鼠的摄食行为

IF 2.5 3区医学

Neuropeptides Pub Date : 2024-10-01 Epub Date: 2024-07-03 DOI: 10.1016/j.npep.2024.102454

Neda Rafiei , Caitlin S. Mitchell , Caitlin R. Tedesco , Jessica Chen , Eun A. Choi , Stephanie Roughley , Philip Jean-Richard-dit-Bressel , Natasha N. Kumar , Gavan P. McNally , Herbert Herzog , Denovan P. Begg

{"title":"Chemogenetic activation ofarcuate nucleus NPY and NPY/AgRP neurons increases feeding behaviour in mice","authors":"Neda Rafiei , Caitlin S. Mitchell , Caitlin R. Tedesco , Jessica Chen , Eun A. Choi , Stephanie Roughley , Philip Jean-Richard-dit-Bressel , Natasha N. Kumar , Gavan P. McNally , Herbert Herzog , Denovan P. Begg","doi":"10.1016/j.npep.2024.102454","DOIUrl":"https://doi.org/10.1016/j.npep.2024.102454","url":null,"abstract":"<div><p>Neuropeptide Y (NPY) plays a crucial role in controlling energy homeostasis and feeding behaviour. The role of NPY neurons located in the arcuate nucleus of the hypothalamus (Arc) in responding to homeostatic signals has been the focus of much investigation, but most studies have used AgRP promoter-driven models, which do not fully encompass Arc NPY neurons. To directly investigate NPY-expressing versus AgRP-expressing Arc neurons function, we utilised chemogenetic techniques in NPY-Cre and AgRP-Cre animals to activate Arc NPY or AgRP neurons in the presence of food and food-related stimuli. Our findings suggest that chemogenetic activation of the broader population of Arc NPY neurons, including AgRP-positive and AgRP-negative NPY neurons, has equivalent effects on feeding behaviour as activation of Arc AgRP neurons. Our results demonstrate that these Arc NPY neurons respond specifically to caloric signals and do not respond to non-caloric signals, in line with what has been observed in AgRP neurons. Activating Arc NPY neurons significantly increases food consumption and influences macronutrient selection to prefer fat intake.</p></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"107 ","pages":"Article 102454"},"PeriodicalIF":2.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141543415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0