Neuropeptides最新文献

{"title":"Bioactive peptides as multipotent molecules bespoke and designed for Alzheimer's disease","authors":"Ana Mesias,&nbsp;Sandra Borges,&nbsp;Manuela Pintado,&nbsp;Sara Baptista-Silva","doi":"10.1016/j.npep.2025.102515","DOIUrl":"10.1016/j.npep.2025.102515","url":null,"abstract":"<div><div>In an increasingly aging world where neurodegenerative diseases (NDs) are exponentially rising, research into more effective and innovative treatments seems paramount. Bioactive peptides (BPs) emerge as promising compounds with revolutionary potential in the treatment of NDs, particularly in well-known conditions like Alzheimer's disease (AD). The biological potential of these compounds is primarily attributed to their drug development advantages such as enhanced penetration, low toxicity, and rapid clearance, as well as, their antioxidant, and anti-inflammatory properties bio-linked to the neuroprotective effect, able to attenuate the multifactorial pathologies of AD. BPs can be sourced from common dietary origins, like animals, plants, marine, and from emerging sources like edible insects. However, to isolate an active BP with beneficial biological effects it must first be released from its parent protein, followed by a synthesis-flow. While <em>in silico</em> approaches can predict a BP's potential bioactivity and structural characteristics, <em>in vitro</em>, cell-based, and <em>in vivo</em> assays should be conducted to ensure these properties. The blood-brain-barrier (BBB) microenvironment and permeability in health or disease state are key factors to consider since they can limit the ability of circulating therapeutical agents, including BPs, to reach the brain. This review focuses on the bioactivity properties of BPs from different dietary protein sources and explores their beneficial effect and neuroprotective activity in AD, unraveling new paths of treatment.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"111 ","pages":"Article 102515"},"PeriodicalIF":2.5,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143563444","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}

{"title":"Ginsenoside Rg1 improves autophagy dysfunction to ameliorate Alzheimer's disease via targeting FGR proto-oncogene","authors":"Qiankun Quan ,&nbsp;Xinxin Ma ,&nbsp;JianJun Feng ,&nbsp;Wanni Li ,&nbsp;Xi Li","doi":"10.1016/j.npep.2025.102514","DOIUrl":"10.1016/j.npep.2025.102514","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a neurodegeneration driven by beta-amyloid (Aβ) deposits in the brain involving autophagy dysfunction. Ginsenoside Rg1, a pharmacologically active compound found in ginseng, has possible therapeutic effects for AD. This study discovered that FGR proto-oncogene (FGR) was a therapeutic target of Rg1 in AD and it was possibly involved in autophagy. C57BL/6 J mice were injected with 5 μL (1 μg/mL) Aβ_1–42 in the right lateral ventricle to establish an AD model. AD mouse hippocampus had high FGR expression. Intragastrically administered Rg1 (40 mg/kg) decreased FGR protein levels in AD mice's hippocampus and improved memory function in AD mice. Both sides of the mice hippocampal fissure were administered with 2 μL lentiviral particles (1 × 10⁷ TU) containing FGR overexpression plasmids. FGR overexpression rendered Rg1 ineffectual in restoring memory function and reducing hippocampal neuron damage. We injected 2 μL lentiviral particles (1 × 10⁷ TU) containing short hairpin RNA plasmids targeting FGR to the mice hippocampal fissures. FGR knockdown improved spatial memory function of AD mice, reduced hippocampal neuron apoptosis, and prevented Aβ accumulation. HT22 cells were transfected with small interfering RNA targeting FGR. FGR knockdown increased the viability of Aβ_1–42 treated HT22 cells. BACE1 and LC3II/I protein levels were decreased and p62 and SIRT1 were increased in AD mice and cells with FGR knockdown. LC3 was down-regulated after inhibiting FGR expression in Aβ_1–42 treated hippocampal neurons. In conclusion, Rg1 exerts anti-AD functions by targeting FGR and downregulating its expression.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"111 ","pages":"Article 102514"},"PeriodicalIF":2.5,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143592338","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}

{"title":"BDNF-mediated depressor response by direct baroreceptor activation benefits for prevention and control of hypertension in high-latitude cold region","authors":"Yan Feng ,&nbsp;Lei Yin ,&nbsp;Ying Li","doi":"10.1016/j.npep.2025.102506","DOIUrl":"10.1016/j.npep.2025.102506","url":null,"abstract":"<div><div>Brian-derived neurotrophic factor (BDNF)-tyrosine kinase B (TrkB) signaling impacts on neuronal and cardiovascular physiology; however, its role in neurocontrol of circulation via baroreflex afferent pathway is largely unknown. Gene and protein expression of BDNF/TrkB were detected in the nodose (NG) and nucleus of tractus solitary (NTS) and expression levels were higher in male compared with female rats, which is relevant well with the blood pressure (BP, males &gt; females in average). Microinjection of BDNF into NG dose-dependently reduced BP and this reduction was more dramatic in shamed control vs. renovascular hypertension (RVH) model rats, which partially inhibited in the presence of TrkB inhibitor K252a, indicating that BDNF-TrkB tends to lower BP under physiological and hypertensive conditions due presumably to a negative feed-back control by BP or compensatory mechanism. To answer this question, expression profiles for BDNF-TrkB were tested in the tissue of NG and NTS collected from RVH model rats. Consistently, the expression of both BDNF-TrkB were significantly up-regulated in RVH model alone with the elevation of BP. Taken these data together, our observation provides direct evidence showing the fundamental role of BDNF-TrkB signaling in autonomic control of BP regulation through baroreflex afferent function, potentially dominant role of BDNF-TrkB-mediated BP reduction in vivo baroreceptor activation due to distinct cellular mechanism compared with their role in the NTS, which extends our understanding of activity-dependent or compensatory mechanism of BDNF-TrkB in response to BP change, and sheds new light of BDNF-TrkB as potential target in prevention and control of hypertension in cold-region.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"111 ","pages":"Article 102506"},"PeriodicalIF":2.5,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143534406","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}

{"title":"Mechanistic role of proteins and peptides in Management of Neurodegenerative Disorders","authors":"Saumya Awasthi ,&nbsp;Prafulla Chandra Tiwari ,&nbsp;Srishti Awasthi ,&nbsp;Arpit Dwivedi ,&nbsp;Shikha Srivastava","doi":"10.1016/j.npep.2025.102505","DOIUrl":"10.1016/j.npep.2025.102505","url":null,"abstract":"<div><div>Proteins and peptides have emerged as significant contributors in the management of neurodegenerative disorders due to their diverse biological functions. These biomolecules influence various cellular processes, including cellular repair, inflammation reduction, and neuronal survival, which are crucial for mitigating the effects of diseases such as Alzheimer's, Parkinson's, and Amyotrophic Lateral Sclerosis (ALS). By interacting with specific cellular receptors, proteins and peptides like neurotrophic factors, cytokines, and enzyme inhibitors promote neurogenesis, reduce oxidative stress, and enhance synaptic plasticity. Nevertheless, till certain limitations and challenges do exist to deliver these fragile therapeutic bioactives. Moreover, targeted delivery systems, such as nanoparticles and biomolecular carriers, are being developed to improve the bioavailability and specificity of these protein-based therapeutics, ensuring efficient crossing of the blood-brain barrier. This review explores the mechanistic pathways through which these biomolecules act, emphasizing their potential to modify disease progression and improve the quality of life in patients with neurodegenerative conditions. Overall, proteins and peptides are not only seen as promising therapeutic agents but also as foundational tools in advancing personalized medicine in the field of neurodegenerative disorders.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"110 ","pages":"Article 102505"},"PeriodicalIF":2.5,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143420506","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}

{"title":"Modulation of temporoammonic-CA1 synapses by neuropeptide Y is through Y1 receptors in mice","authors":"Mariana A. Cortes ,&nbsp;Aundrea F. Bartley ,&nbsp;Qin Li ,&nbsp;Taylor R. Davis ,&nbsp;Stephen E. Cunningham ,&nbsp;Mary Anne Garner ,&nbsp;Patric J. Perez ,&nbsp;Adela C. Harvey ,&nbsp;Alecia K. Gross ,&nbsp;Lynn E. Dobrunz","doi":"10.1016/j.npep.2025.102504","DOIUrl":"10.1016/j.npep.2025.102504","url":null,"abstract":"<div><div>Reduced levels of neuropeptide Y (NPY), an abundant neuromodulator in the brain, are linked to multiple neuropsychiatric disorders, including post-traumatic stress disorder (PTSD). The CA1 region of hippocampus is important for anxiety regulation and highly expresses NPY. Injecting NPY into CA1 is anxiolytic and alleviates behavioral symptoms in a model of traumatic stress; these anxiolytic effects are blocked by a Y1 receptor antagonist. However the location of Y1Rs that mediate NPY's anxiolytic effects in CA1 remains unclear. CA1 receives inputs from entorhinal cortex through the temporammonic pathway (TA), which is important for fear learning and sensitive to stress. Our lab previously showed that NPY reduces TA-evoked synaptic responses, however, the subtype of NPY receptor mediating this reduction is unknown. Here we demonstrate that in mice both exogenous (bath-applied) and endogenously-released NPY act through Y1 receptors in the TA pathway. This is the first demonstration of Y1 receptor-mediated effect on synaptic function in CA1. Interestingly, chronic overexpression of NPY (in NPY-expressing interneurons) impairs the sensitivity of the TA-evoked synaptic response to a Y1 receptor agonist. However, the long-known NPY Y2 receptor-mediated effect on the Schaffer collateral (SC) pathway is unaffected by NPY overexpression. Therefore, NPY can have a pathway-specific impact on synaptic transmission in CA1 based on the differential expression of NPY receptors and their response to overexpression of NPY. Our results demonstrating that NPY acts at Y1 receptors in the TA pathway are consistent with the idea that the TA pathway underlies the anxiolytic effects of NPY in CA1.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"110 ","pages":"Article 102504"},"PeriodicalIF":2.5,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143402962","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}

{"title":"The effects of corticotropin-releasing factor (CRF) and urocortins on the serotonin (hydroxytryptamine, 5HT) released from the raphe nuclei (RN)","authors":"Aliz Kovács ,&nbsp;Patrícia Tancsics ,&nbsp;Miklós Palotai ,&nbsp;Zsolt Bagosi","doi":"10.1016/j.npep.2025.102503","DOIUrl":"10.1016/j.npep.2025.102503","url":null,"abstract":"<div><div>Corticotropin-releasing factor (CRF) and urocortins (UCN1, UCN2 and UCN3) belong to the same CRF family of neuropeptides. They regulate the neuroendocrine, autonomic and behavioral responses to stress <em>via</em> two CRF receptors (CRF1 and CRF2). Stress, anxiety and depression affects the activity of the hypothalamic-pituitary-adrenal (HPA) axis and the serotoninergic neurotransmission, both being regulated by CRF and CRF-related peptides. However, the exact action of CRF and urocortins on the serotonin (5-hydroxytryptamine, 5HT) release was not fully elucidated yet. Therefore, the aim of the present study was to investigate the actions of CRF and urocortins on the 5HT released from the rat raphe nuclei (RN), the most important brain regions producing 5HT, and the participation of CRF receptors in these actions. In order to do so, male Wistar rats were used, their RN were isolated and dissected, and the RN slices were incubated with tritium-labelled 5HT, superfused and stimulated electrically. During superfusion, the RN slices were treated with CRF, UCN1, UCN2 or UCN3, and, when significant effect was observed, pretreated with selective CRF1 antagonist antalarmin or selective CRF2 antagonist astressin2B. The release of tritium-labelled 5HT from the RN was determined by liquid scintillation counting. CRF and UCN1 decreased significantly the tritium-labelled 5HT release from the RN, and these effects were reversed by antalarmin, but not by astressin2B. In addition, UCN3, but not UCN2, increased significantly the tritium-labelled 5HT release from the RN, and this effect was reduced by astressin2B, but not antalarmin. Our results indicate the existence of two apparently opposing CRF systems in the RN: activation of CRF1 by CRF and UCN1 may inhibit, whereas activation of CRF2 by UCN3 may stimulate the 5HT release. The dysbalance between CRF1 and CRF2 activation and, consequently, alteration of serotoninergic signalling may result in anxiety and depression, associated with hyperactivity of the HPA axis.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"110 ","pages":"Article 102503"},"PeriodicalIF":2.5,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971772","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}

{"title":"Sucralose uses reward pathways to promote acute caloric intake","authors":"Qiao-Ping Wang ,&nbsp;An-Qi Li ,&nbsp;Bei Wang ,&nbsp;Xin-Yuan Zhao ,&nbsp;Sha-Sha Li ,&nbsp;Herbert Herzog ,&nbsp;G. Gregory Neely","doi":"10.1016/j.npep.2025.102502","DOIUrl":"10.1016/j.npep.2025.102502","url":null,"abstract":"<div><div>Non-nutritive sweeteners (NNSs) are used to reduce caloric intake by replacing sugar with compounds that are sweet but contain little or no calories. In this study, we investigate how non-nutritive sweetener sucralose to promote acute food intake in the fruit fly <em>Drosophila melanogaster</em>. Our results showed that acute exposure to NNSs sweetness induces a robust hyperphagic response in flies. Cellular and molecular dissection of this acute effect revealed the requirement of a reward pathway comprising of sweet taste neurons, octopaminergic neurons, and NPF neurons which drive increased food intake in response to sucralose. These data provide mechanistic insight into how NNSs can increase food intake, information that may help us better understand how artificially sweeteners may impact our physiology.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"110 ","pages":"Article 102502"},"PeriodicalIF":2.5,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142966180","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}

{"title":"Transcranial pulsed current stimulation alleviates neuronal pyroptosis and neurological dysfunction following traumatic brain injury via the orexin-A/NLRP3 pathway","authors":"Peng Yao ,&nbsp;Qianhui Zhou ,&nbsp;Bingkai Ren ,&nbsp;Li Yang ,&nbsp;Yang Bai ,&nbsp;Zhen Feng","doi":"10.1016/j.npep.2025.102501","DOIUrl":"10.1016/j.npep.2025.102501","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) is a life-threatening condition with high incidence and mortality rates. The current pharmacological interventions for TBI exhibit limited efficacy, underscoring the necessity to explore novel and effective therapeutic approaches to ameliorate its impact. Previous studies have indicated that transcranial pulsed current stimulation (tPCS) can improve neurofunctional deficits in patients by modulating brain neuroplasticity. However, the exact mechanism underlying this neuroprotective effect remains elusive. In this study, mice with TBI induced by controlled cortical impact were subjected to 30 min of daily tPCS for 5 consecutive days and intraperitoneally administered an orexin receptor type 1 (OX₁R) antagonist (SB334867). The neuroprotective effects of tPCS and its potential mechanisms were assessed through behavioral tests, histopathological examination, immunohistochemistry and Western blotting. In vitro experiments involved stimulating HT22 cells with LPS + ATP to assess the anti-neuroinflammatory effects of Orexin-A (OX-A) using CCK-8, Western blotting, and Flow cytometry. The results demonstrated that tPCS reduced the mNSS in TBI mice, ameliorated tissue damage, improved motor and cognitive deficits, and upregulated OX-A expression. Notably, SB334867 reversed the protective effects of tPCS. In vitro studies revealed that OX-A inhibited the formation and activation of NLRP3 inflammasomes, resulting in reduced levels of ROS and restoration of MMP. However, this effect could be reversed by the NLRP3 agonist BMS-986299. Our findings suggest that tPCS promotes the release of OX-A and modulates the OX₁R/NLRP3 pathway to mitigate the inflammatory response following TBI, thereby exerting neuroprotective effects.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"110 ","pages":"Article 102501"},"PeriodicalIF":2.5,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143137317","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}

{"title":"The impact of endogenous N/OFQ on DPN: Insights into lower limb blood flow regulation in rats","authors":"Yuan-jing Qin ,&nbsp;Po Zhang ,&nbsp;Peng Zhang ,&nbsp;Jing Li ,&nbsp;Qixing Yang ,&nbsp;Jun-li Sun ,&nbsp;Yu-zhang Liang ,&nbsp;Li-li Wang ,&nbsp;Lin-zhong Zhang ,&nbsp;Yi Han","doi":"10.1016/j.npep.2024.102492","DOIUrl":"10.1016/j.npep.2024.102492","url":null,"abstract":"<div><div>Diabetic peripheral neuropathy (DPN) is a common complication of diabetes, often accompanied by impaired vascular endothelial function in the lower limbs. This dysfunction is characterized by a reduced vasodilatory response, leading to decreased blood flow in the lower limbs and ultimately contributing to the development of diabetic peripheral neuropathy. To delve deeper into this pathological process, the study employed bioinformatics to identify and analyze genes highly active in DPN. The investigation revealed that Membrane metallo-endopeptidase (MME) was effectively mitigated by its antagonist. Male Sprague-Dawley (SD) rats served as the model to systematically explore the intrinsic connection among the nociceptible/orphanin FQ-N/OFQ receptor (N/OFQ-NOP) system, femoral artery blood flow in the lower extremities, MME, and DPN. The rats were randomized into two groups: a control group and a DPN group induced by a single intraperitoneal injection of 55 mg/kg streptozotocin (STZ), with 6 rats in each group. The findings indicated that compared to the control group, the DPN group exhibited a significant reduction in femoral artery blood flow. This was accompanied by a notable increase in serum N/OFQ concentration, heightened expression of opioid-related nociceptive protein receptor 1 (OPRL1) and MME in femoral artery tissues of the lower limbs, and an elevated sciatic nerve stimulation threshold. These results suggest that the serum N/OFQ level in DPN rats is increased, which may promote the occurrence of peripheral neuropathy by up regulating MME and reducing peripheral flow distribution.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"109 ","pages":"Article 102492"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792147","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}

{"title":"FMRFamide G protein-coupled receptors (GPCR) in the cuttlefish Sepiella japonica: Identification, characterization and expression profile","authors":"Jian-jun Xie ,&nbsp;Ying Li ,&nbsp;Jun-hong Wu,&nbsp;Pei-xuan Fang,&nbsp;Shuang Li,&nbsp;Xu Zhou,&nbsp;Chang-feng Chi","doi":"10.1016/j.npep.2024.102491","DOIUrl":"10.1016/j.npep.2024.102491","url":null,"abstract":"<div><div>FMRFamide is a ubiquitous neuromodulator in the animal kingdom. Once FMRFamide or similar neuropeptides bind to their G protein-coupled receptors (GPCR), a series of signal transduction events are triggered, thereby mediating various physiological effects. FMRFamide had been reported to be involved in the regulation of sexual maturation in <em>Sepiella japonica</em>. In this research, the full-length cDNA of <em>FMRFamide G protein-coupled receptor of S. japonica</em> (<em>SjFaGPCR</em>) was cloned. The sequence is 1396 bp long and encodes a protein consisting of 418 amino acid residues, lacking a signal peptide at the N-terminal region. The 3D structure of <em>Sj</em>FaGPCR was predicted using <em>Todarodes pacificus</em> rhodopsin as a template, and the result indicated the presence of seven transmembrane regions. Multiple sequence alignments and phylogenetic trees indicated that <em>Sj</em>FaGPCR is conserved among invertebrates, and shares highly similar sequence characteristics with other cephalopods. <em>In situ</em> hybridization (ISH) results revealed that significant signals of <em>SjFaGPCR</em> were detected in the central medulla and the granular layer cells of the optic lobe, and were also observed in the supraesophageal and subesophageal masses of the brain<em>.</em> Meanwhile, quantitative real-time PCR (qRT-PCR) results showed that a higher expression level of <em>SjFaGPCR</em> mRNA was detected in the brain and optic lobe of female cuttlefish at stage III and stage VI, and also in the brain (stage V) and optic lobe (stages IV and V) of male cuttlefish than that in other tissues. The co-localization results demonstrated that fluorescence signals of <em>Sj</em>FMRFamide and <em>Sj</em>FaGPCR were overlapped in HEK293 cells, suggesting a possible interaction between the <em>Sj</em>FMRFamide and <em>Sj</em>FaGPCR. These findings provide molecular support for further exploring the roles of FMRFamide and FaGPCR in the reproductive regulation of <em>S. japonica</em>.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"109 ","pages":"Article 102491"},"PeriodicalIF":2.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770728","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}