Pub Date : 2016-01-01DOI: 10.1080/23262133.2016.1235525
Cong Luo, Y. Ikegaya, R. Koyama
ABSTRACT Microglia are recognized as major immune cells in the brain. They have been traditionally studied in various contexts of disease, where their activation has been assumed to induce mostly detrimental effects. Recent studies, however, have challenged the current view of microglia, clarifying their essential contribution to the development of neural circuits and brain function. In this review, we particularly discuss the role of microglia as the major orchestrators that regulate adult neurogenesis in the hippocampus. We also review the roles of microglia in seizure-induced adult neurogenesis in the epileptic dentate gyrus. Specifically, we introduce our recent study, in which we identified a novel mechanism by which viable newborn cells in the adult dentate gyrus are phagocytosed and eliminated by microglia after status epilepticus, maintaining homeostasis of the dentate circuitry. This review aims to reconsider the microglial function in adult neurogenesis, especially when they are activated during epileptogenesis, challenging the dogma that microglia are harmful neurotoxic cells.
{"title":"Microglia and neurogenesis in the epileptic dentate gyrus","authors":"Cong Luo, Y. Ikegaya, R. Koyama","doi":"10.1080/23262133.2016.1235525","DOIUrl":"https://doi.org/10.1080/23262133.2016.1235525","url":null,"abstract":"ABSTRACT Microglia are recognized as major immune cells in the brain. They have been traditionally studied in various contexts of disease, where their activation has been assumed to induce mostly detrimental effects. Recent studies, however, have challenged the current view of microglia, clarifying their essential contribution to the development of neural circuits and brain function. In this review, we particularly discuss the role of microglia as the major orchestrators that regulate adult neurogenesis in the hippocampus. We also review the roles of microglia in seizure-induced adult neurogenesis in the epileptic dentate gyrus. Specifically, we introduce our recent study, in which we identified a novel mechanism by which viable newborn cells in the adult dentate gyrus are phagocytosed and eliminated by microglia after status epilepticus, maintaining homeostasis of the dentate circuitry. This review aims to reconsider the microglial function in adult neurogenesis, especially when they are activated during epileptogenesis, challenging the dogma that microglia are harmful neurotoxic cells.","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2016.1235525","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59994564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1080/23262133.2016.1230167
D. Wiens
ABSTRACT Perinatal dietary supplementation, together with widespread fortification of grain-based foods with synthetic folic acid (FA) has resulted in rising concentrations of unmetabolized plasma FA in pregnant women. In a recently published study we reported on experiments in which we cultured dorsal root ganglia from chick embryos in a range of FA concentrations. We found that FA inhibited neurite extension, synaptogenesis, and growth cone motility. In this commentary we consider the possible mechanism further. The effect of FA is more likely to be on motility processes of growth cones with their exploratory filapodia than on neurotrophic stimulation. Receptors present in the filapodia membrane recognize and bind to environmental guidance cues. The presence of the NMDA receptor on filapodia, and the possible competition of FA with the neurotransmitter glutamate for binding to it, resulting in perturbation of growth cone guidance, are discussed. Whether excess FA exerts its inhibitory effects by such binding competition or via some other mechanism, further investigation is needed. Sufficient intake of folate from conception through the first month of human pregnancy is essential for neural tube closure. However, our results suggest that an upper limit for FA consumption after the first month should be considered.
{"title":"Could folic acid influence growth cone motility during the development of neural connectivity?","authors":"D. Wiens","doi":"10.1080/23262133.2016.1230167","DOIUrl":"https://doi.org/10.1080/23262133.2016.1230167","url":null,"abstract":"ABSTRACT Perinatal dietary supplementation, together with widespread fortification of grain-based foods with synthetic folic acid (FA) has resulted in rising concentrations of unmetabolized plasma FA in pregnant women. In a recently published study we reported on experiments in which we cultured dorsal root ganglia from chick embryos in a range of FA concentrations. We found that FA inhibited neurite extension, synaptogenesis, and growth cone motility. In this commentary we consider the possible mechanism further. The effect of FA is more likely to be on motility processes of growth cones with their exploratory filapodia than on neurotrophic stimulation. Receptors present in the filapodia membrane recognize and bind to environmental guidance cues. The presence of the NMDA receptor on filapodia, and the possible competition of FA with the neurotransmitter glutamate for binding to it, resulting in perturbation of growth cone guidance, are discussed. Whether excess FA exerts its inhibitory effects by such binding competition or via some other mechanism, further investigation is needed. Sufficient intake of folate from conception through the first month of human pregnancy is essential for neural tube closure. However, our results suggest that an upper limit for FA consumption after the first month should be considered.","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2016.1230167","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59994290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1080/23262133.2016.1250034
N. Akizu, M. Martínez-Balbás
ABSTRACT During early stages of neural development, neuroepithelial cells translocate their nuclei along the apicobasal axis in a harmonized manner with the cell cycle. How cell cycle progression and neuroepithelium polarity are coordinated remains unclear. It has been proposed that developmental cues, epigenetic mechanisms and cell cycle regulators must be linked in order to orchestrate these processes. We have recently discovered that a master epigenetic factor, EZH2 is essential to coordinate these events. EZH2 directly represses the cell cycle regulator p21WAF1/CIP in the chicken spinal cord. By doing so, EZH2 controls neural progenitor cell renewal and fine-tunes Rho signaling pathway, which is essential to maintain neuroepithelial structure. Our findings point to a new role of EZH2 during development that could have potential implication in other areas as cancer.
{"title":"EZH2 orchestrates apicobasal polarity and neuroepithelial cell renewal","authors":"N. Akizu, M. Martínez-Balbás","doi":"10.1080/23262133.2016.1250034","DOIUrl":"https://doi.org/10.1080/23262133.2016.1250034","url":null,"abstract":"ABSTRACT During early stages of neural development, neuroepithelial cells translocate their nuclei along the apicobasal axis in a harmonized manner with the cell cycle. How cell cycle progression and neuroepithelium polarity are coordinated remains unclear. It has been proposed that developmental cues, epigenetic mechanisms and cell cycle regulators must be linked in order to orchestrate these processes. We have recently discovered that a master epigenetic factor, EZH2 is essential to coordinate these events. EZH2 directly represses the cell cycle regulator p21WAF1/CIP in the chicken spinal cord. By doing so, EZH2 controls neural progenitor cell renewal and fine-tunes Rho signaling pathway, which is essential to maintain neuroepithelial structure. Our findings point to a new role of EZH2 during development that could have potential implication in other areas as cancer.","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2016.1250034","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59994733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1080/23262133.2016.1231495
Ping Wang, Dejian Zhao, Shira Rockowitz, D. Zheng
ABSTRACT Neural and brain development in human and other mammalian species are largely similar, but distinct features exist at the levels of macrostructure and underlying genetic control. Comparative studies of epigenetic regulation and transcription factor (TF) binding in humans, chimpanzees, rodents, and other species have found large differences in gene regulatory networks. A recent analysis of the cistromes of REST/NRSF, a critical transcriptional regulator for the nervous system, demonstrated that REST binding to syntenic genomic regions (i.e., conserved binding) represents only a small percentage of the total binding events in human and mouse embryonic stem cells. While conserved binding is significantly associated with functional features (e.g., co-factor recruitment) and enriched at genes important for neural development and function, >3000 genes, including many related to brain and neural functions, either contain extra REST-bound sites (e.g., NRXN1) or are targeted by REST only (e.g. PSEN2) in humans. Surprisingly, several genes known to have critical roles in learning and memory, or brain disorders (e.g., APP and HTT) exhibit characteristics of human specific REST regulation. These findings indicate that more systematic studies are needed to better understand the divergent wiring of regulatory networks in humans, mice, and other mammals and their functional implications.
{"title":"Divergence and rewiring of regulatory networks for neural development between human and other species","authors":"Ping Wang, Dejian Zhao, Shira Rockowitz, D. Zheng","doi":"10.1080/23262133.2016.1231495","DOIUrl":"https://doi.org/10.1080/23262133.2016.1231495","url":null,"abstract":"ABSTRACT Neural and brain development in human and other mammalian species are largely similar, but distinct features exist at the levels of macrostructure and underlying genetic control. Comparative studies of epigenetic regulation and transcription factor (TF) binding in humans, chimpanzees, rodents, and other species have found large differences in gene regulatory networks. A recent analysis of the cistromes of REST/NRSF, a critical transcriptional regulator for the nervous system, demonstrated that REST binding to syntenic genomic regions (i.e., conserved binding) represents only a small percentage of the total binding events in human and mouse embryonic stem cells. While conserved binding is significantly associated with functional features (e.g., co-factor recruitment) and enriched at genes important for neural development and function, >3000 genes, including many related to brain and neural functions, either contain extra REST-bound sites (e.g., NRXN1) or are targeted by REST only (e.g. PSEN2) in humans. Surprisingly, several genes known to have critical roles in learning and memory, or brain disorders (e.g., APP and HTT) exhibit characteristics of human specific REST regulation. These findings indicate that more systematic studies are needed to better understand the divergent wiring of regulatory networks in humans, mice, and other mammals and their functional implications.","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":"5743"},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2016.1231495","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59994877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1080/23262133.2016.1253363
Paola Lepanto, José L. Badano, F. R. Zolessi
ABSTRACT The generation of new neurons involves a great variety of cell-extrinsic and cell-intrinsic signals. The primary cilium, long regarded as an “evolutionary vestige,” has emerged as an essential signaling hub in many cells, including neural progenitors and differentiating neurons. Most progenitors harbor an apically-localized primary cilium, which is assembled and disassembled following the cell cycle, while the presence, position and length of this organelle appears to be even more variable in differentiating neurons. One of the main extracellular cues acting through the cilium is Sonic Hedgehog, which modulates spatial patterning, the progression of the cell cycle and the timing of neurogenesis. Other extracellular signals appear to bind to cilia-localized receptors and affect processes such as dendritogenesis. All the observed dynamics, as well as the many signaling pathways depending on cilia, indicate this organelle as an important structure involved in neurogenesis.
{"title":"Neuron's little helper: The role of primary cilia in neurogenesis","authors":"Paola Lepanto, José L. Badano, F. R. Zolessi","doi":"10.1080/23262133.2016.1253363","DOIUrl":"https://doi.org/10.1080/23262133.2016.1253363","url":null,"abstract":"ABSTRACT The generation of new neurons involves a great variety of cell-extrinsic and cell-intrinsic signals. The primary cilium, long regarded as an “evolutionary vestige,” has emerged as an essential signaling hub in many cells, including neural progenitors and differentiating neurons. Most progenitors harbor an apically-localized primary cilium, which is assembled and disassembled following the cell cycle, while the presence, position and length of this organelle appears to be even more variable in differentiating neurons. One of the main extracellular cues acting through the cilium is Sonic Hedgehog, which modulates spatial patterning, the progression of the cell cycle and the timing of neurogenesis. Other extracellular signals appear to bind to cilia-localized receptors and affect processes such as dendritogenesis. All the observed dynamics, as well as the many signaling pathways depending on cilia, indicate this organelle as an important structure involved in neurogenesis.","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2016.1253363","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59994780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1080/23262133.2016.1231160
H. De Jesús-Cortés, A. Rajadhyaksha, A. Pieper
ABSTRACT Neuropsychiatric disease is the leading cause of disability in the United States, and fourth worldwide.1,2 Not surprisingly, human genetic studies have revealed a common genetic predisposition for many forms of neuropsychiatric disease, potentially explaining why overlapping symptoms are commonly observed across multiple diagnostic categories. For example, the CACNA1C gene was recently identified in the largest human genome-wide association study to date as a risk loci held in common across 5 major forms of neuropsychiatric disease: bipolar disorder, schizophrenia, major depressive disorder (MDD), autism spectrum disorder and attention deficit-hyperactivity disorder.3 This gene encodes for the Cav1.2 subunit of the L-type voltage-gated calcium channel (LTCC), accounting for 85% of LTCCs in the brain, while the Cav1.3 subunit comprises the remainder.4 In neurons, LTCCs mediate calcium influx in response to membrane depolarization,5 thereby regulating neurotransmission and gene expression. Here, we describe our recent finding that Cav1.2 also controls survival of young hippocampal neurons in the adult brain, which has been linked to the etiology and treatment of neuropsychiatric disease. We also describe the effective restoration of young hippocampal neuron survival in adult Cav1.2 forebrain-specific conditional knockout mice using the neuroprotective compound P7C3-A20.
{"title":"Cacna1c: Protecting young hippocampal neurons in the adult brain","authors":"H. De Jesús-Cortés, A. Rajadhyaksha, A. Pieper","doi":"10.1080/23262133.2016.1231160","DOIUrl":"https://doi.org/10.1080/23262133.2016.1231160","url":null,"abstract":"ABSTRACT Neuropsychiatric disease is the leading cause of disability in the United States, and fourth worldwide.1,2 Not surprisingly, human genetic studies have revealed a common genetic predisposition for many forms of neuropsychiatric disease, potentially explaining why overlapping symptoms are commonly observed across multiple diagnostic categories. For example, the CACNA1C gene was recently identified in the largest human genome-wide association study to date as a risk loci held in common across 5 major forms of neuropsychiatric disease: bipolar disorder, schizophrenia, major depressive disorder (MDD), autism spectrum disorder and attention deficit-hyperactivity disorder.3 This gene encodes for the Cav1.2 subunit of the L-type voltage-gated calcium channel (LTCC), accounting for 85% of LTCCs in the brain, while the Cav1.3 subunit comprises the remainder.4 In neurons, LTCCs mediate calcium influx in response to membrane depolarization,5 thereby regulating neurotransmission and gene expression. Here, we describe our recent finding that Cav1.2 also controls survival of young hippocampal neurons in the adult brain, which has been linked to the etiology and treatment of neuropsychiatric disease. We also describe the effective restoration of young hippocampal neuron survival in adult Cav1.2 forebrain-specific conditional knockout mice using the neuroprotective compound P7C3-A20.","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2016.1231160","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59994865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1080/23262133.2016.1249195
Kazumi Hirano, M. Namihira
ABSTRACT The cerebral cortex of primates has evolved massively and intricately in comparison to that of other species. Accumulating evidence indicates that this is caused by changes in cell biological features of neural stem cells (NSCs), which differentiate into neurons and glial cells during development. The fate of NSCs during rodent cortical development is stringently regulated by epigenetic factors, such as histone modification enzymes, but the role of these factors in human corticogenesis is largely unknown. We have recently discovered that a lysine-specific demethylase 1 (LSD1), which catalyzes the demethylation of methyl groups in the histone tail, plays a unique role in human fetal NSCs (hfNSCs). We show that, unlike the role previously reported in mice, LSD1 in hfNSCs is necessary for neuronal differentiation and controls the expression of HEYL, one of the NOTCH target genes, by modulating the methylation level of histones on its promoter region. Interestingly, LSD1-regulation of Heyl expression is not observed in mouse NSCs. Furthermore, we first demonstrated that HEYL is able to maintain the undifferentiated state of hfNSCs. Our findings provide a new insight indicating that LSD1 may be a key player in the development and characterization of the evolved cerebral cortex.
{"title":"New insight into LSD1 function in human cortical neurogenesis","authors":"Kazumi Hirano, M. Namihira","doi":"10.1080/23262133.2016.1249195","DOIUrl":"https://doi.org/10.1080/23262133.2016.1249195","url":null,"abstract":"ABSTRACT The cerebral cortex of primates has evolved massively and intricately in comparison to that of other species. Accumulating evidence indicates that this is caused by changes in cell biological features of neural stem cells (NSCs), which differentiate into neurons and glial cells during development. The fate of NSCs during rodent cortical development is stringently regulated by epigenetic factors, such as histone modification enzymes, but the role of these factors in human corticogenesis is largely unknown. We have recently discovered that a lysine-specific demethylase 1 (LSD1), which catalyzes the demethylation of methyl groups in the histone tail, plays a unique role in human fetal NSCs (hfNSCs). We show that, unlike the role previously reported in mice, LSD1 in hfNSCs is necessary for neuronal differentiation and controls the expression of HEYL, one of the NOTCH target genes, by modulating the methylation level of histones on its promoter region. Interestingly, LSD1-regulation of Heyl expression is not observed in mouse NSCs. Furthermore, we first demonstrated that HEYL is able to maintain the undifferentiated state of hfNSCs. Our findings provide a new insight indicating that LSD1 may be a key player in the development and characterization of the evolved cerebral cortex.","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2016.1249195","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59994717","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1080/23262133.2016.1235938
Yosuke Ogura, Y. Sasakura
ABSTRACT The morphogenetic movement associated with neural tube closure (NTC) requires both positive and negative regulations of cell proliferation. The dual requirement of cell division control during NTC underscores the importance of the developmental control of cell division. In the chordate ascidian, midline fusions of the neural ectoderm and surface ectoderm (SE) proceed in the posterior-to-anterior direction, followed by a single wave of asynchronous and patterned cell division in SE. Before NTC, SE exhibits synchronous mitoses; disruption of the synchrony causes a failure of NTC. Therefore, NTC is the crucial turning point at which SE switches from synchronous to patterned mitosis. Our recent work discovered that the first sign of patterned cell division in SE appears was an asynchronous S-phase length along the anterior-posterior axis before NTC: the asynchrony of S-phase is offset by the compensatory G2-phase length, thus maintaining the apparent synchrony of cell division. By the loss of compensatory G2 phase, the synchronized cell division harmoniously switches to a patterned cell division at the onset of NTC. Here we review the developmental regulation of rate and pattern of cell division during NTC with emphasis on the switching mechanism identified in our study.
{"title":"Switching the rate and pattern of cell division for neural tube closure","authors":"Yosuke Ogura, Y. Sasakura","doi":"10.1080/23262133.2016.1235938","DOIUrl":"https://doi.org/10.1080/23262133.2016.1235938","url":null,"abstract":"ABSTRACT The morphogenetic movement associated with neural tube closure (NTC) requires both positive and negative regulations of cell proliferation. The dual requirement of cell division control during NTC underscores the importance of the developmental control of cell division. In the chordate ascidian, midline fusions of the neural ectoderm and surface ectoderm (SE) proceed in the posterior-to-anterior direction, followed by a single wave of asynchronous and patterned cell division in SE. Before NTC, SE exhibits synchronous mitoses; disruption of the synchrony causes a failure of NTC. Therefore, NTC is the crucial turning point at which SE switches from synchronous to patterned mitosis. Our recent work discovered that the first sign of patterned cell division in SE appears was an asynchronous S-phase length along the anterior-posterior axis before NTC: the asynchrony of S-phase is offset by the compensatory G2-phase length, thus maintaining the apparent synchrony of cell division. By the loss of compensatory G2 phase, the synchronized cell division harmoniously switches to a patterned cell division at the onset of NTC. Here we review the developmental regulation of rate and pattern of cell division during NTC with emphasis on the switching mechanism identified in our study.","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2016.1235938","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59994614","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01DOI: 10.1080/23262133.2016.1240055
Hiromu Monai, H. Hirase
ABSTRACT Transcranial direct current stimulation (tDCS) has been reported to be effective for alleviation of neuropsychiatric and neurological conditions as well as enhancement of memory and cognition. Despite the positive effects of tDCS in humans, its mechanism of action remains poorly understood. Recently, we reported that astrocytes, a major glial cell type in the brain, show an increase in intracellular Ca2+ levels during tDCS in the cerebral cortex of the awake mouse. This tDCS-induced elevation in astrocytic Ca2+ has subsequently been demonstrated to be important for cortical plasticity. In this commentary article, we discuss possible interpretations and implications of our findings from the viewpoint of neuron-glia interactions.
{"title":"Astrocytic calcium activation in a mouse model of tDCS—Extended discussion","authors":"Hiromu Monai, H. Hirase","doi":"10.1080/23262133.2016.1240055","DOIUrl":"https://doi.org/10.1080/23262133.2016.1240055","url":null,"abstract":"ABSTRACT Transcranial direct current stimulation (tDCS) has been reported to be effective for alleviation of neuropsychiatric and neurological conditions as well as enhancement of memory and cognition. Despite the positive effects of tDCS in humans, its mechanism of action remains poorly understood. Recently, we reported that astrocytes, a major glial cell type in the brain, show an increase in intracellular Ca2+ levels during tDCS in the cerebral cortex of the awake mouse. This tDCS-induced elevation in astrocytic Ca2+ has subsequently been demonstrated to be important for cortical plasticity. In this commentary article, we discuss possible interpretations and implications of our findings from the viewpoint of neuron-glia interactions.","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2016.1240055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"59994628","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-01-01Epub Date: 2016-01-13DOI: 10.1080/23262133.2015.1127310
Brent Asrican, Patricia Paez-Gonzalez, Joshua Erb, Chay T Kuo
New neuron addition via continued neurogenesis in the postnatal/adult mammalian brain presents a distinct form of nervous system plasticity. During embryonic development, precise temporal and spatial patterns of neurogenesis are necessary to create the nervous system architecture. Similar between embryonic and postnatal stages, neurogenic proliferation is regulated by neural stem cell (NSC)-intrinsic mechanisms layered upon cues from their local microenvironmental niche. Following developmental assembly, it remains relatively unclear what may be the key driving forces that sustain continued production of neurons in the postnatal/adult brain. Recent experimental evidence suggests that patterned activity from specific neural circuits can also directly govern postnatal/adult neurogenesis. Here, we review experimental findings that revealed cholinergic modulation, and how patterns of neuronal activity and acetylcholine release may differentially or synergistically activate downstream signaling in NSCs. Higher-order excitatory and inhibitory inputs regulating cholinergic neuron firing, and their implications in neurogenesis control are also considered.
{"title":"Cholinergic Circuit Control of Postnatal Neurogenesis.","authors":"Brent Asrican, Patricia Paez-Gonzalez, Joshua Erb, Chay T Kuo","doi":"10.1080/23262133.2015.1127310","DOIUrl":"https://doi.org/10.1080/23262133.2015.1127310","url":null,"abstract":"<p><p>New neuron addition via continued neurogenesis in the postnatal/adult mammalian brain presents a distinct form of nervous system plasticity. During embryonic development, precise temporal and spatial patterns of neurogenesis are necessary to create the nervous system architecture. Similar between embryonic and postnatal stages, neurogenic proliferation is regulated by neural stem cell (NSC)-intrinsic mechanisms layered upon cues from their local microenvironmental niche. Following developmental assembly, it remains relatively unclear what may be the key driving forces that sustain continued production of neurons in the postnatal/adult brain. Recent experimental evidence suggests that patterned activity from specific neural circuits can also directly govern postnatal/adult neurogenesis. Here, we review experimental findings that revealed cholinergic modulation, and how patterns of neuronal activity and acetylcholine release may differentially or synergistically activate downstream signaling in NSCs. Higher-order excitatory and inhibitory inputs regulating cholinergic neuron firing, and their implications in neurogenesis control are also considered.</p>","PeriodicalId":74274,"journal":{"name":"Neurogenesis (Austin, Tex.)","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/23262133.2015.1127310","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"34602630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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