Journal of Neuroendocrinology最新文献

{"title":"Proteomic analysis of plasma proteins during fentanyl withdrawal in ovariectomized female rats with and without estradiol.","authors":"Patricia Sinclair, Navdeep S Dhanjal, E Blair Towers, Wendy J Lynch, Nadine Kabbani","doi":"10.1111/jne.70033","DOIUrl":"https://doi.org/10.1111/jne.70033","url":null,"abstract":"<p><p>Evidence from both clinical and preclinical studies indicates that females experience a faster progression to drug addiction and more severe addiction-related health effects compared with males. Estradiol (E2) plays a critical role in these sex differences. Recently, we demonstrated that E2 significantly exacerbates adverse health effects, such as respiratory distress and weight loss, in ovariectomized (OVX) female rats during withdrawal from extended-access fentanyl self-administration. To uncover the mechanisms behind E2-enhanced toxicity, we investigated proteomic changes in the plasma of fentanyl-withdrawn OVX rats under both E2 and non-E2 presentation conditions.Plasma samples were collected following extended-access fentanyl self-administration during protracted withdrawal, when adverse health effects were most pronounced. Using liquid chromatography coupled with electrospray ionization tandem mass spectrometry (LC-ESI MS/MS) we conducted proteomic analysis in OVX rats comparing the effect of fentanyl withdrawal, with or without E2, to drug-naïve control rats.We found a significant effect of fentanyl withdrawal on plasma proteomes within OVX rats. Fentanyl withdrawal was associated with a significant change in 15 plasma proteins including B-factor, properdin (Cfb), apolipoprotein E (ApoE), complement 4, precursor (C4), C-reactive protein (Crp), zinc-alpha-2-glycoprotein precursor (Azgp1), and serine peptidase inhibitor 3L (Serinpa3l). The addition of E2 was associated with enhanced proteomic changes. Bioinformatic gene ontology enrichment analysis indicates that fentanyl withdrawal can disrupt the expression of proteins associated with immunity, lipid transport, and components of the extracellular matrix. We identify protein changes in plasma that may contribute to adverse health outcomes in females, with and without E2, during fentanyl withdrawal. These findings support the development of targeted strategies addressing health risks during opioid use disorder in women.</p>","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70033"},"PeriodicalIF":3.3,"publicationDate":"2025-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143970328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroendocrine mechanisms responsible for elevated gonadotrophin-releasing hormone and luteinising hormone pulses in polycystic ovary syndrome.","authors":"Aleisha M Moore","doi":"10.1111/jne.70028","DOIUrl":"https://doi.org/10.1111/jne.70028","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is the leading cause of anovulatory infertility in premenopausal individuals with ovaries worldwide. Despite the diagnostic features of anovulation, ovarian cysts, and hyperandrogenemia, which indicate that ovary dysfunction is the cause of the syndrome, changes in central neuroendocrine circuits are a significant cause of PCOS pathology. Specifically, cells in the hypothalamus have a diminished ability to transmit negative feedback signals from gonadal sex steroid hormones to gonadotropin-releasing hormone (GnRH) neurons. This results in an elevated frequency of pulsatile hypothalamic GnRH and pituitary luteinizing hormone (LH) secretion, leading to ovarian hyperandrogenism and ovulatory dysfunction. In recent years, preclinical research in animal models has rapidly advanced our understanding of the neural mechanisms underlying GnRH pulse generation with the identification of KNDy cells-a unique cell population in the hypothalamus expressing the neuropeptides kisspeptin, neurokinin B and dynorphin. As a result, therapeutics targeting KNDy cell signaling have emerged as a promising avenue for treating GnRH/LH hypersecretion in PCOS patients. However, the precise central changes underpinning impaired negative feedback regulation of GnRH pulse generation in PCOS patients are still unclear. Evidence from both the clinic and animal models suggests that changes in the regulation of KNDy cells may be directly responsible for elevated GnRH and LH pulse frequency in PCOS. However, other cell populations regulating GnRH secretion may also be involved. This review provides an overview of our current understanding of the aetiology and contribution of neuroendocrine dysfunction in PCOS pathology. It also examines the evidence for neural mechanisms underlying GnRH/LH hypersecretion, which may serve as central targets in developing novel treatments. Finally, this review highlights key knowledge gaps that are hindering the development of preventive and curative interventions.</p>","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70028"},"PeriodicalIF":3.3,"publicationDate":"2025-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144018096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increase of astrocyte apposition on GnRH neurons in early puberty onset induced by high fat diet.","authors":"Isabelle Rodrigues-Santos, Raoni Conceição Dos-Santos, Aline de Jesus, Rafael Appel Flores, Roberta Ribeiro Costa Rosales, Izabela Facco Caliman, Janete A Anselmo-Franci, José Antunes-Rodrigues, Lucila Leico K Elias","doi":"10.1111/jne.70029","DOIUrl":"https://doi.org/10.1111/jne.70029","url":null,"abstract":"<p><p>Puberty onset is driven by the activation of GnRH-secreting neurons and can be advanced by obesity. Astrocytes are dynamic cells that react to changes in the central nervous system environment and participate in the regulation of energy balance and reproduction. To assess the interaction of GnRH neurons and hypothalamic astrocytes during the puberty transition in HFD-treated mice, female and male mice were divided into three groups according to the diet offered at weaning: 42% high-fat diet (HFD42%), 60% high-fat diet (HFD60%), or regular diet (CHOW). The effects of HFD on reproductive tissue and fat content during the prepubertal and pubertal transition were assessed. The impact of HFD on astrocyte interaction with GnRH neurons in the medial preoptic area (MPOA) and arcuate/median eminence (ARC/ME) was assessed. HFD anticipated the first signs of puberty in both male and female mice. Furthermore, there was an increase in adipose and reproductive tissue content in early pubertal animals. Remarkably, the anticipation of puberty onset in females treated with HFD was associated with an increase in the astrocyte apposition on GnRH neurons in the MPOA. Also, there was an increase in astrocyte apposition on GnRH neurons and their fiber projections in the ARC/ME. This study suggests that the HFD-induced anticipation of puberty seems to be, at least partially, mediated by an increase in the morphological association between astrocytes and GnRH neurons in both the MPOA and ARC/EM, which may increase the excitability of GnRH neurons.</p>","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70029"},"PeriodicalIF":3.3,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144012214","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to abstract title \"Efficacy and safety of [177Lu]Lu-edotreotide vs. everolimus in patients with grade 1 or grade 2 gastroenteropancreatic neuroendocrine tumours: COMPETE phase 3 trial\".","authors":"","doi":"10.1111/jne.70025","DOIUrl":"https://doi.org/10.1111/jne.70025","url":null,"abstract":"","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70025"},"PeriodicalIF":3.3,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764033","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prognostic value of clinical parameters and exosomal lncRNA NEAT1_1 in MEN1-related non-functioning pancreatic neuroendocrine tumors.","authors":"Jerena Manoharan, Max Albers, Natalia Khizanishvili, Norman Krasser-Gercke, Maxime Schmitt, Ioannis Mintziras, Sabine Wächter, Anja Rinke, Yutong Gao, Jörg W Bartsch, Moritz Jesinghaus, Pietro Di Fazio, Detlef K Bartsch","doi":"10.1111/jne.70024","DOIUrl":"https://doi.org/10.1111/jne.70024","url":null,"abstract":"<p><p>Non-functioning pancreatic neuroendocrine tumors (NF-pNETs) significantly contribute to the premature death of multiple endocrine neoplasia type 1 (MEN1) patients. Reliable prognostic markers are not yet available. MicroRNAs (miRNA) and long-non-coding (lnc) RNAs, transported by extracellular vesicles, are emerging as new prognostic tools. This study aimed to analyze the clinical characteristics, the exosomal-miRNA 451 (exo-miR451) and the lnc-RNA nuclear paraspeckle assembly transcript 1 (NEAT1_1, 3.7 kB) in the mild and aggressive courses of MEN1-NFpNET disease. Patient characteristics were assessed regarding an aggressive course of disease. In addition, exo-miR451 and exo-lnc-NEAT1_1 expression levels were quantified in serum by RT-qPCR and correlated with clinical data. Immunohistochemistry results of STAT3 (signal transducer and activator of transcription 3), regulated by NEAT1, were performed in NF-pNET tissue and correlated with exo-lnc-NEAT1_1 expression. Among 66 MEN1 patients with NF-pNETs, 13 (20%) had an aggressive disease course. No significant differences in patient characteristics were observed between those with aggressive (n = 13) and mild (n = 53) disease (all p > .5). Exosomal miRNA-451 was dysregulated in 55% (n = 23) of cases, showing a trend toward higher upregulation in the aggressive group (36% vs. 19%), although this difference was not statistically significant (p = .215). Exo-NEAT1_1 was overexpressed in 42% (16/38) of patients, without significant differences between groups (p = .0523). However, exo-NEAT1_1 expression strongly correlated with STAT3 immunohistochemical staining (p = .001). Although no prognostic marker could be identified, we show for the first time that the STAT3-NEAT1 pathway plays a role in MEN1-associated NF-pNET tumorigenesis.</p>","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70024"},"PeriodicalIF":3.3,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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 feminization hormone therapy on the brain of transgender women: A hypothesis.","authors":"Leire Zubiaurre-Elorza, Carme Uribe, Alberto Marcos, Rosa Fernández, Eduardo Pásaro, Mª Cruz Rodríguez Del Cerro, Sarah M Burke, Antonio Guillamon","doi":"10.1111/jne.70026","DOIUrl":"https://doi.org/10.1111/jne.70026","url":null,"abstract":"<p><p>Gender-affirming hormone therapy (GAHT) is a medical treatment used to help transgender individuals align their physical appearance with their gender identity. GAHT in transgender women (TW) has been found to lead to a reduction in brain tissue with an expansion of the ventricles. We discuss an animal model studying the effects of GAHT that suggests dehydration of brain tissue and an alteration in the relative concentration of brain metabolites. We hypothesize that estradiol, acting on astrocytes, alters cerebral blood flow, water metabolism, and metabolite concentration and argue that these changes could explain the higher risk of stroke observed in GAHT-treated TW compared to untreated cisgender men. Future studies should clarify the mechanisms underlying the brain tissue changes induced by GAHT.</p>","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70026"},"PeriodicalIF":3.3,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143719910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of membrane estrogen receptor alpha on the negative feedback of estrogens on luteinizing hormone secretion.","authors":"Mélanie C Faure, Rebeca Corona, Laura Vandries, Charlotte Deconinck, Françoise Lenfant, Céline Gérard, Jean-Michel Foidart, Charlotte A Cornil","doi":"10.1111/jne.70016","DOIUrl":"https://doi.org/10.1111/jne.70016","url":null,"abstract":"<p><p>Estrogen receptor alpha (ERα) is critical for reproduction, but the relative contributions of its nuclear and membrane signaling are unclear.The present study investigated the role of membrane ERα (mERα) using two complementary approaches: a mouse model lacking mERα signaling (C451A-ERα mice) and estetrol (E₄), a natural estrogen described to prevent membrane ERα activation in different cell types. While ovariectomy (OVX) induced a comparable luteinizing hormone (LH) increase in both wild-type and C451A-ERα females, C451A-ERα females failed to respond to chronic estradiol (E₂) (1 μg) exposure, indicating dysregulated negative feedback. This lack of LH regulation in C451A-ERα females was mirrored by an absence of change in the number of neurons immunoreactive (ir) for kisspeptin (Kp) in both the rostral periventricular area of the third ventricle (RP3V) and the arcuate nucleus (ARC), for progesterone receptor (PR)-ir nuclei in the preoptic area and hypothalamus, and for neurokinin 3 receptor (NK₃R) in the ARC. Interestingly, increasing the dose of E₂ to 5 μg restored normal negative feedback and normal numbers of Kp-ir neurons and PR-ir nuclei, but not the surface covered by Kp-ir fibers and the number of NK₃R-ir neurons in the ARC. By contrast, E₄ mimicked the negative feedback of E₂ on circulating LH in OVX WT females following both acute and chronic treatment and potentiated rather than blocked the effects of E₂ when administered along with it. E₄ also mimicked the stimulatory effects of E₂ on the number of PR-ir nuclei in several preoptic and hypothalamic regions and the percentage of area covered by Kp-ir material in the ARC, as well as its inhibitory action on the number of Kp-ir neurons in the ARC. Therefore, the C451A-ERα mutation interferes with the control of the negative feedback through distinct mechanisms differing by their dose-dependency to E₂. By contrast, E₄ mimicked all effects of E₂ on the negative feedback and the associated neural circuits, indicating that E₄ acts as a weak ERα agonist in this context. Together, these results suggest that C451A-ERα modifies the sensitivity to E₂, impacting the negative feedback of E₂ on LH regulation.</p>","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70016"},"PeriodicalIF":3.3,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early testosterone exposure during development advances myelination and affects neurogenesis of the vocal control motor path in male zebra finches (Taeniopygia guttata).","authors":"Adriana Diez, Kevin G Young, Scott A MacDougall-Shackleton","doi":"10.1111/jne.70022","DOIUrl":"https://doi.org/10.1111/jne.70022","url":null,"abstract":"<p><p>Birdsong learning and production is mediated through a vocal control circuit that exhibits ubiquitous and profound sex differences. In zebra finches (Taeniopygia guttata) only males sing, and sex differences in both neuroanatomy and myelination of this circuit emerge during the first 3 months of life as song learning is taking place. Song crystallization occurs at the onset of sexual maturity, at a time when neuron recruitment to the vocal control region HVC is reduced and the myelination of the projection from HVC to the motor nucleus RA (robust nucleus of arcopallium) rapidly develops. Prior work demonstrated that experimental testosterone treatment early in song development disrupted song learning, potentially by leading to premature song crystallization, but the effects of testosterone on neurogenesis and myelination of the vocal control system are little studied. We implanted male zebra finches with blank or testosterone pellets around Day 35 at the onset of the sensorimotor phase of song development. We examined the effects of early testosterone treatment on song development, myelination, and neurogenesis (doublecortin labeled cells) of the motor path of the vocal control circuit (HVC to RA). We also quantified singing consistency at two ages in adulthood. Testosterone treatment accelerated changes in myelin within HVC and in the projection from HVC to RA and accelerated age-related changes in doublecortin-labeled cells in HVC. Song and syllable stereotypy increased with age, but we did not detect an effect of hormone treatment. These results are consistent with the hypothesis that the testosterone exposure during development initiates processes that normally occur at sexual maturity, including changes in neurogenesis and myelination of the motor control path of the vocal control system.</p>","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70022"},"PeriodicalIF":3.3,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corticosteroid-regulated gene transcription in SH-SY5Y-derived neurons: Insights into the mineralocorticoid and glucocorticoid receptor-mediated response.","authors":"Justina F Lugenbühl, Clara Snijders, Cameron D Pernia, Marina Soliva Estruch, Gunter Kenis, Nikolaos P Daskalakis","doi":"10.1111/jne.70021","DOIUrl":"https://doi.org/10.1111/jne.70021","url":null,"abstract":"<p><p>Post-traumatic stress disorder (PTSD) and major depressive disorder (MDD) are debilitating stress-related psychiatric disorders that can develop following exposure to traumatic events or chronic stress in some individuals. The neurobiological processes leading to disease remain largely unknown. Among others, these disorders are characterized by a dysregulated hypothalamic-pituitary-adrenal axis, which is regulated by the glucocorticoid receptor (GR) and the mineralocorticoid receptor (MR). This leads to altered downstream corticosteroid-induced gene expression. In vitro models are promising tools to investigate specific neurobiological underpinnings of the stress response in the brain. Here, we investigated the suitability of SH-SY5Y-derived neurons as a cost-efficient system to study the role of GR and MR in the neuronal stress response. SH-SY5Y-derived neurons were characterized, exposed to corticosteroids, and analyzed on transcriptomic and proteomic levels. We show that (i) these neurons express sufficient and seemingly functional GR and MR to allow the study of corticosteroid-induced transcription, (ii) three corticosteroids cortisol, dexamethasone, and aldosterone, induced similar transcriptomic effects, (iii) the antagonist spironolactone mildly attenuated the effects of dexamethasone in FKBP5, DUSP1, and SUPV3L1. Mifepristone did not significantly alter the effect of aldosterone. (iv) Integrating transcriptomic alterations of these corticosteroid-exposed neurons with those of iPSC-derived neurons exposed to dexamethasone showed concordant corticosteroid-induced effects in the two in vitro systems. To determine translational validity, we compared the gene expression in these neurons with the transcriptome of postmortem brain samples from individuals with PTSD and MDD, yielding stronger negative correlations of corticosteroid effects in SH-SY5Y-derived neurons with PTSD signatures than with MDD signatures. Upon further refinement and validation, SH-SY5Y-derived neurons may serve as a simplistic tool to study neuronal corticosteroid-induced gene expression and the implicated molecular networks around GR and MR. Strengthening our insight into these receptors' functions improves our understanding of the hypothalamic-pituitary-adrenal axis, which is commonly altered in stress-related psychiatric disorders such as PTSD and MDD.</p>","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70021"},"PeriodicalIF":3.3,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Seasonal regulation of Tsh-β, Dio2, Dio3, and GnRH-I mRNA expressions in Eurasian tree sparrow (Passer montanus) under natural conditions.","authors":"Bidisha Kataki, Anand S Dixit","doi":"10.1111/jne.70023","DOIUrl":"https://doi.org/10.1111/jne.70023","url":null,"abstract":"<p><p>Seasonal transitions in avian reproductive cycles are governed by neuroendocrine adaptability. The molecular mechanisms behind seasonal regulation are still not fully understood in many species and remain an important area of ongoing research. Despite recognizing the importance of regulatory genes, gaps persist in comprehending the exact molecular processes that control the transitions between different reproductive phases. We investigated the expression patterns of Tsh-β (Thyroid-stimulating hormone subunit beta), Dio2 (Iodothyronine deiodinase 2), Dio3 (Iodothyronine deiodinase 3), and GnRH-I (Gonadotropin-releasing hormone I) mRNAs in regulating reproduction in both sexes of the Eurasian tree sparrow (Passer montanus). Adult tree sparrows (n = 4 for each sex) were procured from the wild, and mRNA expression of Tsh-β, Dio2, Dio3, and GnRH-I, along with gonadal size and body weight, was examined on a monthly basis for 1 year. Results revealed distinct annual cycles of Tsh-β, Dio2, Dio3, and GnRH-I mRNA expression and gonadal size in both sexes. Significantly higher expressions of Tsh-β, Dio2, and GnRH-I mRNA were observed during the breeding phase (April-May), while Dio3 expression was reported higher during the non-breeding phase. The synchronization in the pattern of increase in the Tsh-β, Dio2, and GnRH-I during the breeding phase is associated with gonadal growth, suggesting their potential involvement in regulating seasonal reproduction in tree sparrows. Thus, the control of the reproductive cycle in tree sparrows involves the actions of Tsh-β and Dio2/Dio3 leading to the activation and deactivation of GnRH-I via the HPG (hypothalamic-pituitary-gonadal) axis.</p>","PeriodicalId":16535,"journal":{"name":"Journal of Neuroendocrinology","volume":" ","pages":"e70023"},"PeriodicalIF":3.3,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143663752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}