Pub Date : 2024-11-17DOI: 10.1016/j.yfrne.2024.101162
Shakeera L Walker, Erica R Glasper
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 from parental neglect.
{"title":"Unraveling sex differences in maternal and paternal care impacts on social behaviors and neurobiological responses to early-life adversity.","authors":"Shakeera L Walker, Erica R Glasper","doi":"10.1016/j.yfrne.2024.101162","DOIUrl":"https://doi.org/10.1016/j.yfrne.2024.101162","url":null,"abstract":"<p><p>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 from parental neglect.</p>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":" ","pages":"101162"},"PeriodicalIF":6.5,"publicationDate":"2024-11-17","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}
Pub Date : 2024-11-12DOI: 10.1016/j.yfrne.2024.101161
Cellas A. Hayes , Destiny Wilson , Miguel A. De Leon , Mubarak Jolayemi Mustapha , Sharon Morales , Michelle C. Odden , Nicole M. Ashpole
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.
{"title":"Insulin-like growth factor-1 and cognitive health: Exploring cellular, preclinical, and clinical dimensions","authors":"Cellas A. Hayes , Destiny Wilson , Miguel A. De Leon , Mubarak Jolayemi Mustapha , Sharon Morales , Michelle C. Odden , 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":"2024-11-12","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}
Progesterone is a highly lipophilic gonadal hormone that can influence behavior and mental health through its receptors in the brain. Fluctuations in progesterone levels across critical periods of a females life are associated with increased susceptibility to mental conditions.
This review highlights the effects of progestagens, including progesterone and synthetic progestins, on the brain, mood, stress, and cognition in females. The primary focus is on experimental pharmacological research that teases out the distinct effects of progestagens from those of estrogens. Additionally, the key literature on puberty, the menstrual cycle, pregnancy, perimenopause, hormonal contraceptives, and menopausal hormone therapy is reviewed, although conclusions are limited by the nested effects of progestagens and estrogens.
Single study-findings suggest an influence of progesterone on amygdala reactivity related to processing of emotional stimuli and memory. In patients with premenstrual dysphoric disorder, progesterone receptor modulation improves premenstrual mood symptoms and potentially enhances fronto-cingulate control over emotion processing. The interaction between progestagens and the systems involved in the regulation of stress seems to influence subjective experiences of mood and stress. Sparse studies investigating the effects of progestin-only contraceptives suggest effects of progestagens on the brain, mood, and stress. Progesterone and progestins used for contraception can influence neural processes as myelination and neuroprotection, exerting protective effects against stroke. Concerning menopausal hormonal therapy, the effects of progestins are largely unknown.
Levels of progesterone as well as type, administration route, timing, dose regimen, metabolism, and intracellular activity of progestins in hormonal contraceptives and menopausal hormonal therapy are factors whose effects remain to be elucidated. Altogether, current knowledge highlights the potential role of progestagens in females health but also calls for well-designed pharmaco-behavioral studies disentangling the effects of progestagens from those of estrogens.
{"title":"Progestagens and progesterone receptor modulation: Effects on the brain, mood, stress, and cognition in females","authors":"Celine Bencker , Laura Gschwandtner , Sibel Nayman , Ramunė Grikšienė , Billie Nguyen , Urs M. Nater , Rachida Guennoun , Inger Sundström-Poromaa , Belinda Pletzer , Marie Bixo , Erika Comasco","doi":"10.1016/j.yfrne.2024.101160","DOIUrl":"10.1016/j.yfrne.2024.101160","url":null,"abstract":"<div><div>Progesterone is a highly lipophilic gonadal hormone that can influence behavior and mental health through its receptors in the brain. Fluctuations in progesterone levels across critical periods of a females life are associated with increased susceptibility to mental conditions.</div><div>This review highlights the effects of progestagens, including progesterone and synthetic progestins, on the brain, mood, stress, and cognition in females. The primary focus is on experimental pharmacological research that teases out the distinct effects of progestagens from those of estrogens. Additionally, the key literature on puberty, the menstrual cycle, pregnancy, perimenopause, hormonal contraceptives, and menopausal hormone therapy is reviewed, although conclusions are limited by the nested effects of progestagens and estrogens.</div><div>Single study-findings suggest an influence of progesterone on amygdala reactivity related to processing of emotional stimuli and memory. In patients with premenstrual dysphoric disorder, progesterone receptor modulation improves premenstrual mood symptoms and potentially enhances fronto-cingulate control over emotion processing. The interaction between progestagens and the systems involved in the regulation of stress seems to influence subjective experiences of mood and stress. Sparse studies investigating the effects of progestin-only contraceptives suggest effects of progestagens on the brain, mood, and stress. Progesterone and progestins used for contraception can influence neural processes as myelination and neuroprotection, exerting protective effects against stroke. Concerning menopausal hormonal therapy, the effects of progestins are largely unknown.</div><div>Levels of progesterone as well as type, administration route, timing, dose regimen, metabolism, and intracellular activity of progestins in hormonal contraceptives and menopausal hormonal therapy are factors whose effects remain to be elucidated. Altogether, current knowledge highlights the potential role of progestagens in females health but also calls for well-designed pharmaco-behavioral studies disentangling the effects of progestagens from those of estrogens.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"76 ","pages":"Article 101160"},"PeriodicalIF":6.5,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142617956","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}
Pub Date : 2024-10-01DOI: 10.1016/j.yfrne.2024.101157
Attila Zsarnovszky , Daiana Alymbaeva , Gergely Jocsak , Csaba Szabo , Boglárka Mária Schilling-Tóth , David Sandor Kiss
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.
神经对平衡的调节依赖于健康的突触功能。突触功能对生理需求的适应表现为各种形式的突触可塑性（SP），由正常的激素调节回路调节。在过去几十年中，动物和人类生物体的激素调节已成为数千种化学物质的目标，这些化学物质有可能成为内源性激素的激动剂或拮抗剂。随着这些干扰内分泌的化学品（EDCs）的作用机制成为研究的焦点，越来越多的研究表明，激素的调节途径之一，即 SP 的形态形式，很可能是一种受 EDCs 影响的神经机制。本综述讨论了一些最著名的 EDC 对形态突触可塑性（MSP）的已知和潜在影响。我们强调了被 EDCs 改变的分子机制，并指出在这一神经内分泌学领域越来越需要开展更多的研究。
{"title":"Endocrine disrupting effects on morphological synaptic plasticity","authors":"Attila Zsarnovszky , Daiana Alymbaeva , Gergely Jocsak , Csaba Szabo , Boglárka Mária Schilling-Tóth , 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}
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 trans-synaptic degeneration.
{"title":"Brain alteration of autoimmune thyroid disease: Neuropsychiatric impact, neuroimaging insights, and neurobiological implications","authors":"Qin Wei , Haiyang Zhang , Haixia Guan , Xuefei Song , 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}
Pub Date : 2024-10-01DOI: 10.1016/j.yfrne.2024.101158
Rafael Mineiro , Maria Rodrigues Cardoso , Ana Catarina Duarte , Cecília Santos , Jose Cipolla-Neto , Fernanda Gaspar do Amaral , Diana Costa , Telma Quintela
The blood–brain barrier and the blood-cerebrospinal fluid barrier separate the blood from brain tissue and cerebrospinal fluid. These brain barriers are important to maintain homeostasis and complex functions by protecting the brain from xenobiotics and harmful endogenous compounds. The disruption of brain barriers is a characteristic of neurologic diseases. Melatonin is a lipophilic hormone that is mainly produced by the pineal gland. The blood–brain barrier and the blood-cerebrospinal fluid barriers are melatonin-binding sites. Among the several melatonin actions, the most characteristic one is the regulation of sleep-wake cycles, melatonin has anti-inflammatory and antioxidant properties. Since brain barriers disruption can arise from inflammation and oxidative stress, knowing the influence of melatonin on the integrity of brain barriers is extremely important. Therefore, the objective of this review is to gather and discuss the available literature about the regulation of brain barriers by melatonin.
{"title":"Melatonin and brain barriers: The protection conferred by melatonin to the blood-brain barrier and blood-cerebrospinal fluid barrier","authors":"Rafael Mineiro , Maria Rodrigues Cardoso , Ana Catarina Duarte , Cecília Santos , Jose Cipolla-Neto , Fernanda Gaspar do Amaral , Diana Costa , Telma Quintela","doi":"10.1016/j.yfrne.2024.101158","DOIUrl":"10.1016/j.yfrne.2024.101158","url":null,"abstract":"<div><div>The blood–brain barrier and the blood-cerebrospinal fluid barrier separate the blood from brain tissue and cerebrospinal fluid. These brain barriers are important to maintain homeostasis and complex functions by protecting the brain from xenobiotics and harmful endogenous compounds. The disruption of brain barriers is a characteristic of neurologic diseases. Melatonin is a lipophilic hormone that is mainly produced by the pineal gland. The blood–brain barrier and the blood-cerebrospinal fluid barriers are melatonin-binding sites. Among the several melatonin actions, the most characteristic one is the regulation of sleep-wake cycles, melatonin has anti-inflammatory and antioxidant properties. Since brain barriers disruption can arise from inflammation and oxidative stress, knowing the influence of melatonin on the integrity of brain barriers is extremely important. Therefore, the objective of this review is to gather and discuss the available literature about the regulation of brain barriers by melatonin.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"75 ","pages":"Article 101158"},"PeriodicalIF":6.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142441665","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}
Pub Date : 2024-10-01DOI: 10.1016/j.yfrne.2024.101156
Mélanie Bourque , Marc Morissette , Amandine Isenbrandt , Silvia Giatti , Roberto Cosimo Melcangi , Manolo Carta , Roberto Frau , Marco Bortolato , Denis Soulet , Thérèse Di Paolo
Parkinson’s disease (PD) is characterized by motor symptoms due to loss of brain dopamine and non-motor symptoms, including gastrointestinal disorders. Although there is no cure for PD, symptomatic treatments are available. L-Dopa is the gold standard PD therapy, but most patients develop dyskinesias (LID), which are challenging to manage. Amantadine is recognized as the most effective drug for LID, but its adverse effects limit the use in patients. Here we review how 5α-reductase inhibitors (5ARIs), drugs used to treat benign prostatic hyperplasia and alopecia, exhibit beneficial effects in PD animal models. 5ARIs show neuroprotective properties in brain and gut dopaminergic systems, and reduce dyskinesias in rodent model of PD. Additionally, the 5ARI finasteride dampened dopaminergic-induced drug gambling in PD patients. Neuroprotection and antidyskinetic activities of 5ARIs in animal models of PD suggest their potential repurposing in men with PD to address gut dysfunction, protect brain DA and inhibit dyskinesias.
{"title":"Effect of 5-alpha reductase inhibitors in animal models of Parkinson’s disease","authors":"Mélanie Bourque , Marc Morissette , Amandine Isenbrandt , Silvia Giatti , Roberto Cosimo Melcangi , Manolo Carta , Roberto Frau , Marco Bortolato , Denis Soulet , Thérèse Di Paolo","doi":"10.1016/j.yfrne.2024.101156","DOIUrl":"10.1016/j.yfrne.2024.101156","url":null,"abstract":"<div><div>Parkinson’s disease (PD) is characterized by motor symptoms due to loss of brain dopamine and non-motor symptoms, including gastrointestinal disorders. Although there is no cure for PD, symptomatic treatments are available. L-Dopa is the gold standard PD therapy, but most patients develop dyskinesias (LID), which are challenging to manage. Amantadine is recognized as the most effective drug for LID, but its adverse effects limit the use in patients. Here we review how 5α-reductase inhibitors (5ARIs), drugs used to treat benign prostatic hyperplasia and alopecia, exhibit beneficial effects in PD animal models. 5ARIs show neuroprotective properties in brain and gut dopaminergic systems, and reduce dyskinesias in rodent model of PD. Additionally, the 5ARI finasteride dampened dopaminergic-induced drug gambling in PD patients. Neuroprotection and antidyskinetic activities of 5ARIs in animal models of PD suggest their potential repurposing in men with PD to address gut dysfunction, protect brain DA and inhibit dyskinesias.</div></div>","PeriodicalId":12469,"journal":{"name":"Frontiers in Neuroendocrinology","volume":"75 ","pages":"Article 101156"},"PeriodicalIF":6.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142368190","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}
Pub Date : 2024-09-01DOI: 10.1016/j.yfrne.2024.101155
Ming Li
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-HT2C 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.
{"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 D<sub>1</sub>/D<sub>2</sub> receptors and its stimulating action on serotonin 5-HT<sub>2C</sub> 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":"2024-09-01","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}
Pub Date : 2024-09-01DOI: 10.1016/j.yfrne.2024.101154
Ariane Sharif, Vincent Prevot
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.
{"title":"Astrogenesis in the hypothalamus: A life-long process contributing to the development and plasticity of neuroendocrine networks","authors":"Ariane Sharif, 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":"2024-09-01","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}
Pub Date : 2024-08-10DOI: 10.1016/j.yfrne.2024.101153
Michael V. Ugrumov
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.
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