Frontiers in Neuroendocrinology最新文献

{"title":"The oxytocin system in patients with craniopharyngioma: A systematic review","authors":"Amy Mann ,&nbsp;Jennifer Kalitsi ,&nbsp;Khushali Jani ,&nbsp;Daniel Martins ,&nbsp;Ritika R Kapoor ,&nbsp;Yannis Paloyelis","doi":"10.1016/j.yfrne.2024.101170","DOIUrl":"10.1016/j.yfrne.2024.101170","url":null,"abstract":"<div><div>Craniopharyngioma is a benign tumour affecting the hypothalamic and pituitary regions, which are involved in the production and secretion of oxytocin. We conducted a systematic review to assess dysregulation of the oxytocin system in craniopharyngioma and associations with neurobehavioural, eating, and metabolic abnormalities. Eight studies (n = 72 patients) were included. Evidence for dysfunction of the endogenous oxytocin system in craniopharyngioma is limited and mixed. While no significant differences in baseline salivary oxytocin concentrations were reported between patients with craniopharyngioma and controls, patients with craniopharyngioma were found to have blunted salivary oxytocin response following exercise stimulation and this was associated with greater state anxiety and higher BMI. Studies administering exogenous oxytocin are sparse and do not meet required standards. Hypothalamic damage may pose an additional mechanism of oxytocin dysregulation. Improving understanding of the oxytocin system in craniopharyngioma could be pivotal for exploring the potential therapeutic role of exogenous oxytocin in this condition.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"76 ","pages":"Article 101170"},"PeriodicalIF":6.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142767788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insulin-like growth factor-1 and cognitive health: Exploring cellular, preclinical, and clinical dimensions","authors":"Cellas A. Hayes ,&nbsp;Destiny Wilson ,&nbsp;Miguel A. De Leon ,&nbsp;Mubarak Jolayemi Mustapha ,&nbsp;Sharon Morales ,&nbsp;Michelle C. Odden ,&nbsp;Nicole M. Ashpole","doi":"10.1016/j.yfrne.2024.101161","DOIUrl":"10.1016/j.yfrne.2024.101161","url":null,"abstract":"<div><div>Age and insulin-like growth factor-1 (IGF-1) have an inverse association with cognitive decline and dementia. IGF-1 is known to have important pleiotropic functions beginning in neurodevelopment and extending into adulthood such as neurogenesis. At the cellular level, IGF-1 has pleiotropic signaling mechanisms through the IGF-1 receptor on neurons and neuroglia to attenuate inflammation, promote myelination, maintain astrocytic functions for homeostatic balances, and neuronal synaptogenesis. In preclinical rodent models of aging and transgenic models of IGF-1, increased IGF-1 improves cognition in a variety of behavioral paradigms along with reducing IGF-1 via knockout models being able to induce cognitive impairment. At the clinical levels, most studies highlight that increased levels of IGF-1 are associated with better cognition. This review provides a comprehensive and up-to-date evaluation of the association between IGF-1 and cognition at the cellular signaling levels, preclinical, and clinical levels.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"76 ","pages":"Article 101161"},"PeriodicalIF":6.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling sex differences in maternal and paternal care impacts on social behaviors and neurobiological responses to early-life adversity","authors":"Shakeera L. Walker ,&nbsp;Erica R. Glasper","doi":"10.1016/j.yfrne.2024.101162","DOIUrl":"10.1016/j.yfrne.2024.101162","url":null,"abstract":"<div><div>Early-life stress (ELS) affects the development of prosocial behaviors and social-cognitive function, often leading to structural brain changes and increased psychosocial disorders. Recent studies suggest that mother- and father-child relationships independently influence social development in a sex-specific manner, but the effects of impaired father-child relationships are often overlooked. This review examines preclinical rodent studies to explore how parental neglect impacts neuroplasticity and social behaviors in offspring. We highlight that disruptions in maternal interactions may affect male pups more in uniparental rodents, while impaired paternal interactions in biparental rodents tend to impact female pups more. Due to limited research, the separate effects of maternal and paternal neglect on brain development and social behaviors in biparental species remain unclear. Addressing these gaps could clarify the sex-specific mechanisms underlying social and neurobiological deficits following parental neglect.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"76 ","pages":"Article 101162"},"PeriodicalIF":6.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142675285","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Menstrually-related mood disorders and postpartum depression: Convergent aspects in aetiology","authors":"D. Islas-Preciado ,&nbsp;E. Estrada-Camarena ,&nbsp;L.A.M. Galea","doi":"10.1016/j.yfrne.2024.101171","DOIUrl":"10.1016/j.yfrne.2024.101171","url":null,"abstract":"<div><div>Females diagnosed with Menstrually-related mood disorders (MRMDs) have more risk to develop postpartum depression (PPD). There are overlapping symptoms between MRMDs and PPD such as anxiety, depressed mood, irritability, that can contribute to a lower quality of life. MRMDs and PPD share components in their etiology such as dramatic hormonal oscillations, and alterations in Hypothalamus-Pituitary-Adrenal (HPA) axis activity that may impair GABAergic neurotransmission. As well, stressful events that impact HPA regulation may play an important role in the etiology of MRMDs and PPD. Here we review common hormone fluctuations across the menstrual cycle and pregnancy/postpartum to identify shared pathways that could contribute to greater sensitivity in people with MRMDs and PPD. This review summarizes hormone sensitivity, HPA axis activity and neurosteroids effects on GABAergic transmission and the potential role of chronic stress in developing MRMDs and PPD. In addition, other potential etiopathological factors, such as serotonin and the immune system, are discussed. Investigating the etiopathology of MRMDs and PDD will help to better understand the complexity of factors involved in these disorders that affect females across the reproductive years.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"76 ","pages":"Article 101171"},"PeriodicalIF":6.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142784683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gut feeling: Exploring the intertwined trilateral nexus of gut microbiota, sex hormones, and mental health","authors":"Luana Leao ,&nbsp;Saba Miri ,&nbsp;Riadh Hammami","doi":"10.1016/j.yfrne.2024.101173","DOIUrl":"10.1016/j.yfrne.2024.101173","url":null,"abstract":"<div><div>The complex interplay between the gut microbiota, sex hormones, and mental health is emerging as a pivotal factor in understanding and managing psychiatric disorders. Beyond their traditional roles, sex hormones exert profound effects on various physiological systems including the gut microbiota. Fluctuations in sex hormone levels, notably during the menstrual cycle, influence gut physiology and barrier function, shaping gut microbiota composition and immune responses. Conversely, the gut microbiota actively modulates sex hormone levels via enzymatic processes. This bidirectional relationship underscores the significance of the gut-brain axis in maintaining mental well-being. This review explores the multifaceted interactions between sex hormones, the gut microbiota, and mental health outcomes. We highlight the potential of personalized interventions in treating psychiatric disorders, particularly in vulnerable populations such as premenopausal women and individuals with depressive disorders. By elucidating these complex interactions, we aim to provide insights for future research into targeted interventions, enhancing mental health outcomes.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"76 ","pages":"Article 101173"},"PeriodicalIF":6.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypothalamic neurons fully or partially expressing the dopaminergic phenotype: development, distribution, functioning and functional significance. A review","authors":"Michael V. Ugrumov","doi":"10.1016/j.yfrne.2024.101153","DOIUrl":"10.1016/j.yfrne.2024.101153","url":null,"abstract":"<div><p>The hypothalamus is a key link in neuroendocrine regulations, which are provided by neuropeptides and dopamine. Until the late 1980 s, it was believed that, along with peptidergic neurons, hypothalamus contained dopaminergic neurons. Over time, it has been shown that besides dopaminergic neurons expressing the dopamine transporter and dopamine-synthesizing enzymes − tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC) − the hypothalamus contains neurons expressing only TH, only AADC, both enzymes or only dopamine transporter. The end secretory product of TH neurons is L-3,4-dihydroxyphenylalanine, while that of AADC neurons and bienzymatic neurons lacking the dopamine transporter is dopamine. During ontogenesis, especially in the perinatal period, monoenzymatic neurons predominate in the hypothalamic neuroendocrine centers. It is assumed that L-3,4-dihydroxyphenylalanine and dopamine are released into the neuropil, cerebral ventricles, and blood vessels, participating in the regulation of target cell differentiation in the perinatal period and the functioning of target cells in adulthood.</p></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"75 ","pages":"Article 101153"},"PeriodicalIF":6.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141916535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endocrine disrupting effects on morphological synaptic plasticity","authors":"Attila Zsarnovszky ,&nbsp;Daiana Alymbaeva ,&nbsp;Gergely Jocsak ,&nbsp;Csaba Szabo ,&nbsp;Boglárka Mária Schilling-Tóth ,&nbsp;David Sandor Kiss","doi":"10.1016/j.yfrne.2024.101157","DOIUrl":"10.1016/j.yfrne.2024.101157","url":null,"abstract":"<div><div>Neural regulation of the homeostasis depends on healthy synaptic function. Adaptation of synaptic functions to physiological needs manifests in various forms of synaptic plasticity (SP), regulated by the normal hormonal regulatory circuits. During the past several decades, the hormonal regulation of animal and human organisms have become targets of thousands of chemicals that have the potential to act as agonists or antagonists of the endogenous hormones. As the action mechanism of these endocrine disrupting chemicals (EDCs) came into the focus of research, a growing number of studies suggest that one of the regulatory avenues of hormones, the morphological form of SP, may well be a neural mechanism affected by EDCs. The present review discusses known and potential effects of some of the best known EDCs on morphological synaptic plasticity (MSP). We highlight molecular mechanisms altered by EDCs and indicate the growing need for more research in this area of neuroendocrinology.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"75 ","pages":"Article 101157"},"PeriodicalIF":6.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrogenesis in the hypothalamus: A life-long process contributing to the development and plasticity of neuroendocrine networks","authors":"Ariane Sharif,&nbsp;Vincent Prevot","doi":"10.1016/j.yfrne.2024.101154","DOIUrl":"10.1016/j.yfrne.2024.101154","url":null,"abstract":"<div><p>Astrocytes are now recognized as integral components of neural circuits, regulating their maturation, activity and plasticity. Neuroendocrinology has provided fertile ground for revealing the diverse strategies used by astrocytes to regulate the physiological and behavioural outcomes of neural circuit activity in response to internal and environmental inputs. However, the development of astrocytes in the hypothalamus has received much less attention than in other brain regions such as the cerebral cortex and spinal cord. In this review, we synthesize our current knowledge of astrogenesis in the hypothalamus across various life stages. A distinctive feature of hypothalamic astrogenesis is that it persists all throughout lifespan, and involves multiple cellular sources corresponding to radial glial cells during early development, followed by tanycytes, parenchymal progenitors and locally dividing astrocytes. Astrogenesis in the hypothalamus is closely coordinated with the maturation of hypothalamic neurons. This coordination is exemplified by recent findings in neurons producing gonadotropin-releasing hormone, which actively shape their astroglial environment during infancy to integrate functionally into their neural network and facilitate sexual maturation, a process vulnerable to endocrine disruption. While hypothalamic astrogenesis shares common principles with other brain regions, it also exhibits specific features in its dynamics and regulation, both at the inter- and intra-regional levels. These unique properties emphasize the importance of further exploration. Additionally, we discuss the experimental strategies used to assess astrogenesis in the hypothalamus and their potential bias and limitations. Understanding the mechanisms of hypothalamic astrogenesis throughout life will be crucial for comprehending the development and function of the hypothalamus under both physiological and pathological conditions.</p></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"75 ","pages":"Article 101154"},"PeriodicalIF":6.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0091302224000347/pdfft?md5=a32cadde74f9da395b8daf8afbeaeb3d&pid=1-s2.0-S0091302224000347-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142125326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is melanin-concentrating hormone in the medial preoptic area a signal for the decline of maternal care in late postpartum?","authors":"Ming Li","doi":"10.1016/j.yfrne.2024.101155","DOIUrl":"10.1016/j.yfrne.2024.101155","url":null,"abstract":"<div><p>This manuscript proposes that melanin-concentrating hormone (MCH) in the medial preoptic area (MPOA) is an neurochemical signal evolved to trigger the declining process of maternal care. MCH in the MPOA appears only after parturition and is progressively increased with the progression of lactation, while maternal behavior declines progressively. Intra-MPOA injection of MCH decreases active maternal responses. MCH is also highly responsive to infant characteristics and maternal condition. Behavioral changes induced by MCH in late postpartum period are conducive to the decline of infant-directed maternal behavior. The MPOA MCH system may mediate the maternal behavior decline by suppressing the maternal approach motivation and/or increasing maternal withdrawal via its inhibitory action onto the mesolimbic dopamine D₁/D₂ receptors and its stimulating action on serotonin 5-HT_2C receptors in the ventral tegmental area. Research into the MCH maternal effects will enhance our understanding of the neurochemical mechanisms underlying the maternal behavior decline.</p></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"75 ","pages":"Article 101155"},"PeriodicalIF":6.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain alteration of autoimmune thyroid disease: Neuropsychiatric impact, neuroimaging insights, and neurobiological implications","authors":"Qin Wei ,&nbsp;Haiyang Zhang ,&nbsp;Haixia Guan ,&nbsp;Xuefei Song ,&nbsp;Huifang Zhou","doi":"10.1016/j.yfrne.2024.101159","DOIUrl":"10.1016/j.yfrne.2024.101159","url":null,"abstract":"<div><div>Autoimmune thyroid disease (AITD) is the most common organ-specific autoimmune disease, characterized by thyroid function disorder and autoimmune imbalance. Previous studies have demonstrated the decreased quality of life and neuropsychiatric manifestations in AITD patients, including anxiety, depression, cognitive impairment and affective disorder. These problems also plague the euthyroid AITD patients. Advanced neuroimaging techniques were well carried out and employed as an explanatory instrument for the above intriguing phenomenon. In recent years, an increasing number of neuroimaging studies have reported that these neuropsychiatric manifestations are accompanied by significant structural and functional brain alterations in AITD patients, mainly involved in neurocognitive and emotional regions, despite the underlying neurobiological mechanism is still unclear. The existing studies suggest that the potential pathogenesis of the neuropsychiatric manifestations and brain alterations does not depend on a single factor, but may result from a combination of thyroid function dysfunction, metabolic disorders, dysregulated autoimmune and <em>trans</em>-synaptic degeneration.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"75 ","pages":"Article 101159"},"PeriodicalIF":6.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142566449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}