Neuropeptides最新文献

{"title":"Dynorphin B induces mitochondrial fragmentation in NSCLC through the PKD/DRP-1 signaling pathway","authors":"Yunxiao Li ,&nbsp;Bin Zhou ,&nbsp;Yuenan Yang ,&nbsp;Kexin Liu ,&nbsp;Shichao Zhou","doi":"10.1016/j.npep.2025.102535","DOIUrl":"10.1016/j.npep.2025.102535","url":null,"abstract":"<div><div>Mitochondrial fragmentation and impairment are essential targets for therapeutic approach for non-small cell lung cancer (NSCLC), given their significant contributions to the persistence and progression of malignant cells. Dynorphin B (Dyn B), an endogenous opioid peptide, has been demonstrated for its involvement in an extensive array of cellular activities; however, its specific functions and mechanisms within the context of cancer remain largely undefined. To address this, we employed NCI-H2087 NSCLC cells treated with Dyn B (0.01–100 μM) and utilized lactate dehydrogenase (LDH) release and γ-glutamyl transpeptidase (GPT) activity assays to evaluate cytotoxicity. Mitochondrial function was assessed via Complex I activity assays, adenosine triphosphate (ATP) production measurements, and MitoSOX Green staining for reactive oxygen species (ROS). MitoTracker Red staining with ImageJ quantification characterized mitochondrial morphology, while Western blot analysis probed phosphorylation of dynamin-related protein 1 (DRP1) and protein kinase D (PKD). Lentiviral shRNA-mediated PKD silencing was used to validate functional rescue of mitochondrial dynamics. This investigation reveals that Dyn B induces cytotoxic effects in NCI-H2087 NSCLC cells by facilitating mitochondrial dysfunction and fragmentation. Treatment with Dyn B resulted in a significant augmentation of LDH and elevated GPT activity, indicating cellular injury. Additionally, Dyn B compromised mitochondrial functionality by reducing Complex I activity, diminishing ATP synthesis, and promoting mitochondrial ROS generation. Mechanistically, Dyn B triggered mitochondrial fragmentation through activation of DRP1 and PKD, without affecting protein kinase C (PKC). Silencing of PKD reversed Dyn B–induced mitochondrial fragmentation and restored mitochondrial functionality. These findings underscore the promising role of Dyn B as a prospective therapeutic agent in NSCLC, targeting mitochondrial dynamics via the PKD-DRP1 signaling pathway.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102535"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144517632","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":"Neuropeptide Y as a multifaceted modulator of neuroplasticity, Neuroinflammation, and HPA axis dysregulation: Perceptions into treatment-resistant depression","authors":"Priyanka Singanwad ,&nbsp;Amol Tatode ,&nbsp;Mohammad Qutub ,&nbsp;Brijesh Taksande ,&nbsp;Milind Umekar ,&nbsp;Rashmi Trivedi ,&nbsp;Tanvi Premchandani","doi":"10.1016/j.npep.2025.102538","DOIUrl":"10.1016/j.npep.2025.102538","url":null,"abstract":"<div><div>Treatment-resistant depression (TRD) is a severe neurobiological and clinical category in which common antidepressants do not induce an adequate response. Neuropeptide Y (NPY), a neuropeptide highly conserved through evolution, is known to be involved in the regulation of stress responses, emotional processing, neuroinflammation, and neuroplasticity. This review synthesizes the importance of NPY in TRD by describing NPY's physiological (central nervous system) functions and roles. Experimental data suggest that NPY is dysregulated in animal models of chronic stress and TRD, which include changes in hippocampal NPY signaling, neurotrophic factor expression, and HPA axis activity. Clinical studies have, in turn, shown decreased cerebrospinal NPY concentrations in TRD patients as well as decreased expression of NPY receptors in stress-related regions of their brains. Finally, we discuss new therapeutic avenues targeting NPY pathology, such as intranasal NPY administration and receptor-selective modulation. Thus, preclinical and clinical data jointly suggest that restoration of NPY signaling pathways might offer a novel and biologically grounded intervention for TRD.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102538"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144632410","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":"Rapamycin reveals neuropeptide Y as a regulator of senescence and inflammatory pathways in arthritis","authors":"Susana Aideé González-Chávez ,&nbsp;Eduardo Chaparro-Barrera ,&nbsp;Mario Loya-Rivera ,&nbsp;Alejandra Jazmín Rodríguez-Castillo ,&nbsp;Rodrigo Prieto-Carrasco ,&nbsp;Renato J. Aguilera ,&nbsp;Ana P. Betancourt ,&nbsp;Jonathon E. Mohl ,&nbsp;Daniel Alberto Ruizesparza-Hinojos ,&nbsp;Sergio de Jesús Ramírez-Pérez ,&nbsp;Mercedes Bermúdez ,&nbsp;César Pacheco-Tena","doi":"10.1016/j.npep.2025.102533","DOIUrl":"10.1016/j.npep.2025.102533","url":null,"abstract":"<div><h3>Background</h3><div>Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by immune dysregulation and joint destruction. Cellular senescence has been implicated in the progression of RA through the senescence-associated secretory phenotype (SASP), yet its molecular links to inflammation remain unclear. Rapamycin, an mTOR inhibitor with anti-inflammatory and anti-senescence properties, provides a valuable tool for exploring these mechanisms.</div></div><div><h3>Objective</h3><div>To investigate the link between senescence and inflammation in a murine model of RA by comparing the transcriptome of diseased joints in rapamycin-treated and untreated mice.</div></div><div><h3>Methods</h3><div>Collagen-induced arthritis was established in DBA/1 mice, followed by 40 days of rapamycin treatment. RNA sequencing and bioinformatic analyses were performed to identify differentially expressed genes and altered signaling pathways. RT-qPCR and immunohistochemistry validated candidate genes. Functional assays were conducted in fibroblast-like synoviocytes (FLS) following <em>Npy</em> silencing.</div></div><div><h3>Results</h3><div>Rapamycin treatment reduced the incidence and severity of arthritis while modulating senescence- and autophagy-related pathways. Transcriptomic analysis identified neuropeptide Y (<em>Npy</em>) as a differentially expressed gene linking senescence and inflammation, with reduced protein levels following rapamycin treatment, similar to TNF and β-galactosidase. NPY receptor expression (<em>Npy1r</em> and <em>Npy2r</em>) and autophagy-related genes (<em>Sirt1</em>, <em>Sirt6</em>, and <em>Lc3b</em>) were also modulated in vivo. In vitro, <em>Npy</em> silencing in FLS significantly reduced the expression of the SASP cytokines <em>Tnfa</em>, <em>Il1b</em>, and <em>Il6</em>, downregulated <em>Npy1r</em> and <em>Npy2r</em>, and increased <em>Sirt1</em> expression.</div></div><div><h3>Conclusion</h3><div>This study identifies <em>Npy</em> as a modulator of inflammation and senescence-related pathways in arthritis. Its regulation by rapamycin and impact on sirtuins, autophagy, and NPY receptor expression suggest a broader role in RA pathogenesis.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102533"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144308168","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":"Effects of oxytocin on behavior and neurotrophic factors in the brain of aged female rats exposed to chronic social isolation","authors":"Helin Demirtas ,&nbsp;Burcu Acikgoz ,&nbsp;Ayca Arslankiran ,&nbsp;Bahar Dalkiran ,&nbsp;Amac Kiray ,&nbsp;Muge Kiray ,&nbsp;Ayfer Dayi ,&nbsp;Ilkay Aksu","doi":"10.1016/j.npep.2025.102532","DOIUrl":"10.1016/j.npep.2025.102532","url":null,"abstract":"<div><div>This study aimed to investigate the effects of social isolation stress and intranasally administered oxytocin on physiological and behavioral alterations during aging in rats. A total of 28, aged female Sprague-Dawley rats were allocated into four groups: control (C), social isolation (SI), oxytocin (O), and oxytocin+social isolation (OI). Animals in the SI and OI groups were housed in individual cages for four weeks. Intranasal oxytocin (2 μg/kg/day) was administered to the O and OI groups 14 times during the third and fourth weeks of the study. Behavioral assessments were conducted. Levels of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) were measured. In the Morris water maze test, all groups demonstrated improved learning performance, reflected by a progressive reduction in the time taken to locate the hidden platform. The three-chamber sociability test revealed that sociability was significantly impaired in the SI group but preserved in the O, OI, and C groups. VEGF levels in the prefrontal cortex were significantly reduced in the SI group compared to all other groups. Notably, VEGF levels were higher in the OI group than in the SI group. Hippocampal neuron density was lower in the SI group but was preserved in the OI group, suggesting a neuroprotective effect of oxytocin. These findings highlight the protective roles of oxytocin and sociability against the detrimental effects of chronic social isolation, particularly in preserving hippocampal neuron density and maintaining sociability and learning. Further research is needed to elucidate the molecular and behavioral mechanisms underlying these effects.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102532"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144298115","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":"Tauopathies: Emerging discoveries on tau protein, with a special focus on Alzheimer's disease","authors":"Aishwarya Hattiholi ,&nbsp;Harsha Hegde ,&nbsp;Suhas Kumar Shetty","doi":"10.1016/j.npep.2025.102536","DOIUrl":"10.1016/j.npep.2025.102536","url":null,"abstract":"<div><div>Tauopathies encompass a group of neurodegenerative disorders (NDDs) driven by the abnormal accumulation of mutated tau protein, leading to hyperphosphorylation, neuronal damage, and neuroinflammation. The protein plays essential roles in brain function but undergoes hyperphosphorylation and aggregation into toxic oligomers in NDDs. Recent research emphasizes the need to understand tau's post-translational modifications (PTMs) and their role in pathological states. Insights into tau's structure, isoform-specific properties, and aggregation mechanisms are critical for elucidating its propagation in neurodegeneration. Moreover, tau's potential as a biomarker and the development of targeted therapies to mitigate tauopathies, particularly in AD, remain promising avenues. However, many strategies targeted at tau have repeatedly failed, which continues the search for better alternatives. This review focuses on recent advances in tau research, highlighting its structural and functional characteristics, and roles in disease, that may be critical to understanding their implications for new therapeutic strategies. PTMs are important for the stable structure and physiological functions of a protein. However, dysfunctional PTMs are the leading causes of tau protein aggregation. The recent shift on tau hyperphosphorylation has resulted in many discoveries related to their functions in AD. Therapeutic strategies targeting phosphorylated tau are being extensively studied worldwide. This paper gives a comprehensive view on these aspects.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"112 ","pages":"Article 102536"},"PeriodicalIF":2.5,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144571243","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":"Astrocyte Glucose-6-phosphorylase-Beta regulates ventromedial hypothalamic nucleus glucose counterregulatory neurotransmission and systemic hormone profiles","authors":"Karen P. Briski,&nbsp;Sushma Katakam,&nbsp;Subash Sapkota,&nbsp;Madhu Babu Pasula,&nbsp;Rami Shrestha,&nbsp;Rajesh Vadav","doi":"10.1016/j.npep.2025.102519","DOIUrl":"10.1016/j.npep.2025.102519","url":null,"abstract":"<div><div>Brain astrocytes generate free glucose at the conclusion of glycogenolysis or gluconeogenesis by glucose-6-phosphatase-beta (Glc-6-Pase-<em>β</em>) hydrolytic action. Astrocytes shape ventromedial hypothalamic nucleus (VMN) control of glucose counterregulation via lactate provision, yet possible effects of astrocyte endogenous glucose production are unknown. Current research investigated eu- and hypoglycemic patterns of VMN neuron counterregulatory neurotransmitter marker protein expression and counterregulatory hormone secretion following in vivo VMN astrocyte Glc-6-Pase-<em>β</em> gene-knockdown. Gene-silencing caused reductions in VMN astrocyte Glc-6-Pase-<em>β</em> protein expression and tissue glycogen and glucose content. Hypoglycemic suppression (dorsomedial VMN; VMNdm) or augmentation (ventrolateral VMN; VMNvl) of glycogen involves Glc-6-Pase-<em>β</em> –independent versus -dependent mechanisms, respectively. siRNA pretreatment reversed hypoglycemic down-regulation of VMNdm glucose levels and intensified up-regulated VMNvl glucose accumulation. Glc-6-Pase-<em>β</em> gene-knockdown correspondingly suppressed or enhanced baseline expression of glutamate decarboxylase_65/67 (GAD) and neuronal nitric oxide synthase (nNOS), protein markers for the counterregulation-inhibiting or -enhancing neurochemicals γ-aminobutyric acid and nitric oxide. Glc-6-Pase-<em>β</em> siRNA pretreatment did not alter hypoglycemic suppression of VMN GAD protein but reversed (VMNdm) or amplified (VMNvl) nNOS up-regulation. VMN Glc-6-Pase-<em>β</em> gene-silencing attenuated hypoglycemic patterns of corticosterone and growth hormone secretion and enhanced glucagon release. In summary, data provide unique evidence that VMN Glc-6-Pase-<em>β</em> activity affects glucose counterregulation. Outcomes document astrocyte Glc-6-Pase-<em>β</em> control of VMN glucose and glycogen accumulation as well as VMN neuron counterregulatory neurotransmission. Further research is warranted to identify Glc-6-Pase-<em>β</em> – mediated adjustments in astrocyte glucose metabolism that affect VMN GABAergic and/or nitrergic signaling within the brain glucostatic circuitry.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"111 ","pages":"Article 102519"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143679826","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":"Interaction of glucocorticoids and interleukins in the control of hypothalamic neurohypophysial system output in salt loaded male rats","authors":"R.R. Ventura ,&nbsp;S.G. Ruginsk ,&nbsp;A. Lopes da Silva ,&nbsp;D. Badauê-Passos Jr ,&nbsp;H.D. Francescato ,&nbsp;T.M. Coimbra ,&nbsp;L.L.K. Elias ,&nbsp;J. Antunes-Rodrigues","doi":"10.1016/j.npep.2025.102523","DOIUrl":"10.1016/j.npep.2025.102523","url":null,"abstract":"<div><div>The present study investigated the effects of a 4-day salt load (0.3 M NaCl, SL) and dexamethasone treatment (DEXA, 1 mg/Kg, subcutaneous) on the mechanisms possibly underlying glucocorticoid-mediated effects on hypothalamic neurohypophyseal system (HNS) activity. As expected, SL animals developed hyperosmolality, reflecting the progressive increase in plasma sodium concentrations. SL also triggered increased hypothalamic expression of vasopressin (AVP) and oxytocin (OT) messenger RNAs (mRNAs), increased magnocellular neuronal activation, and enhanced plasma hormone concentrations. Plasma corticosterone, interleukin (IL) 1β and tumor necrosis factor alfa, but not IL-6 levels, were also elevated in response to SL. Increased salt consumption also significantly decreased hypothalamic mRNA expression for the p65 subunit of the nuclear factor kappa B (NFkB), and increased mRNA expression for type β NFkB inhibitory protein (IκBβ). The protein expression ratio between phosphorylated and total NFκB was also elevated in SL rats. DEXA administration, in turn, prevented SL-induced AVP and OT release, as well as decreased corticosterone/IL plasma levels. Therefore, the present results suggest that increased salt consumption may originate a systemic-driven pro-inflammatory response, which can contribute to the increased secretion of corticosterone observed in SL animals. We therefore hypothesize that elevated systemic IL levels, in parallel with corticosterone secretion, may constitute, besides hyperosmolality, important redundant stimuli triggering SL-induced neuropeptide release. Conversely, high levels of corticosterone would produce, in the long term, inhibition of HNS activity and the termination of the neurosecretory response.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"111 ","pages":"Article 102523"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143928148","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":"Regulation of the gut-brain-pituitary-gonad axis in tilapia: Evidence for the involvement of orexin","authors":"Mallikarjun Gouda,&nbsp;C.B. Ganesh","doi":"10.1016/j.npep.2025.102525","DOIUrl":"10.1016/j.npep.2025.102525","url":null,"abstract":"<div><div>The neuropeptide orexin is known as the regulator of appetite and is implicated in many physiological functions in vertebrates. Nevertheless, the physiological importance of this peptide within the gut-brain-reproductive axis remains poorly understood in teleosts. This work aimed at assessing the response of orexin to starvation and its impact on food consumption and the reproductive axis in tilapia. In the first experiment, the fish subjected to 21 days of starvation showed a greater increase in the intensity of orexin-A immunoreactivity in the hypothalamus and pituitary gland compared to controls. The administration of either 0.1 or 1 mg orexin antagonist lemborexant (LBX) for 21 days led to a dose-dependent significant reduction in food intake, whereas a significant increase in the numbers of spermatogenic cells was observed in a high-dose LBX-treated group compared to the control fish. Moreover, a high-dose of LBX significantly enhanced the intensity of androgen receptor protein immunolabelling in the testis, percent area of gonadotropin-releasing hormone (GnRH) immunolabelling in the proximal pars distalis of the pituitary gland (PPD), and the serum levels of luteinizing hormone (LH) and 11-ketotestosterone (11-KT). In addition, the <em>in vitro</em> testicular concentration of 11-KT was significantly increased following a high-dose LBX treatment. Overall, these findings suggest that blockade of orexin receptors by LBX promotes the spermatogenesis process. This effect might be mediated <em>via</em> the stimulation of 11-KT and androgen receptors at the testicular level and the GnRH-LH pathway at the hypothalamic-pituitary level in tilapia.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"111 ","pages":"Article 102525"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144134970","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":"Factors affecting the physical stability of peptide self-assembly in neurodegenerative disorders","authors":"Jahnu Saikia ,&nbsp;Mouli Sarkar ,&nbsp;Vibin Ramakrishnan","doi":"10.1016/j.npep.2025.102517","DOIUrl":"10.1016/j.npep.2025.102517","url":null,"abstract":"<div><div>Biological systems comprise of diverse biomolecules, including proteins, nucleic acids, lipids, and carbohydrates. Peptides, which are short chains of amino acids, exhibit unique properties when assembled to nano-level architectures. Self-assembling peptides possess a remarkable ability to organize into structured aggregates such as nanofibers, nanotubes, nanoribbons, and nanovesicles. These intricate structures are linked to neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, Prion disease, Huntington's disease, and type II diabetes. Peptide nano assembly can be guided by external stimuli, such as temperature, pH, ultrasound, electric and magnetic fields. In this review, the discussion will be centred around the various factors that influence the self-assembly of peptides alongside therapeutic interventions that align with the fundamental principles of thermodynamics and kinetics to modulate the aggregation characteristics of peptide self-assembly.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"111 ","pages":"Article 102517"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670407","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":"Profile of cocaine and amphetamine regulated transcript peptide (CARTp) and Corticotropin-releasing factor (CRF) in the brain of Euphlyctis cyanophlyctis during puddle desiccation","authors":"Swapnil A. Shewale ,&nbsp;Sunil J. Koli ,&nbsp;Sneha Sagarkar ,&nbsp;Ameeta Ravikumar ,&nbsp;Shobha Bhargava","doi":"10.1016/j.npep.2025.102518","DOIUrl":"10.1016/j.npep.2025.102518","url":null,"abstract":"<div><div>During the post breeding season, anuran tadpoles are subjected to a wide range of environmental variables due to intermittent dry spells leading to pond desiccation. To avoid these harsh conditions, anurans accelerate rate of metamorphosis. In anurans, hypothalamic corticotropin-releasing factor (CRF) senses stress and activates metamorphosis via hypothamalo-pituitary- interenal/thyroid axis. Cocaine and amphetamine regulated transcript peptide (CARTp) is widely reported in the brains of vertebrates except reptiles. Role of CARTp along with CRF in mitigating the physiological effects of stress in mammals is well established. Therefore, we investigated effect of puddle desiccation on the CARTp and CRF peptide immunoreactivity in the brain of prometamorphic tadpoles of <em>Euphlyctis cyanophlyctis.</em> Animals in the naturally occurring desiccating puddle were fixed on field and the expression of CARTp and CRF were studied using immunohistochemistry. CARTp-immunoreactivity in entopeduncular nucleus (AEN and PEN), nucleus medialis septi (NMS) and hypothalamus (dHy and vHy) significantly increased in the prometamorphic tadpoles exposed to puddle desiccation as compared to controls. In preoptic area (POA) and Edinger Westphal nucleus (EW) significant increase in CARTp as well as CRF immunoreactive cells were observed in puddle desiccation group. Strong CRF immunoreactivity was observed in median eminence of stressed group. Puddle desiccation induced increase in the expression of CARTp and CRF peptide in the neuroendocrine axis may suggest their involvement in environmental stress induced accelerated metamorphosis. Moreover, elevated expression of CARTp but not CRF peptide in regions regulating energy homeostasis may indicate starvation due to scarcity of food or stress induced appetite suppression.</div></div>","PeriodicalId":19254,"journal":{"name":"Neuropeptides","volume":"111 ","pages":"Article 102518"},"PeriodicalIF":2.5,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670409","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}