LIVIVO - Search results -

Search results

Result 1 - 10 of total 29

Search options

Article: Molecular Mechanisms of Cadherin Function During Cortical Migration.

Martinez-Garay, Isabel

Frontiers in cell and developmental biology

2020 Volume 8, Page(s) 588152

Abstract: During development of the cerebral cortex, different types of neurons migrate from distinct origins to create the different cortical layers and settle within them. Along their way, migrating neurons use cell adhesion molecules on their surface to ... ...

Abstract	During development of the cerebral cortex, different types of neurons migrate from distinct origins to create the different cortical layers and settle within them. Along their way, migrating neurons use cell adhesion molecules on their surface to interact with other cells that will play critical roles to ensure that migration is successful. Radially migrating projection neurons interact primarily with radial glia and Cajal-Retzius cells, whereas interneurons originating in the subpallium follow a longer, tangential route and encounter additional cellular substrates before reaching the cortex. Cell-cell adhesion is therefore essential for the correct migration of cortical neurons. Several members of the cadherin superfamily of cell adhesion proteins, which mediate cellular interactions through calcium-dependent, mostly homophilic binding, have been shown to play important roles during neuronal migration of both projection neurons and interneurons. Although several classical cadherins and protocadherins are involved in this process, the most prominent is CDH2. This mini review will explore the cellular and molecular mechanisms underpinning cadherin function during cortical migration, including recent advances in our understanding of the control of adhesive strength through regulation of cadherin surface levels.
Language	English
Publishing date	2020-09-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2020.588152
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Article: Transcriptional control of embryonic and adult neural progenitor activity.

Singh, Niharika / Siebzehnrubl, Florian A / Martinez-Garay, Isabel

Frontiers in neuroscience

2023 Volume 17, Page(s) 1217596

Abstract: Neural precursors generate neurons in the embryonic brain and in restricted niches of the adult brain in a process called neurogenesis. The precise control of cell proliferation and differentiation in time and space required for neurogenesis depends on ... ...

Abstract	Neural precursors generate neurons in the embryonic brain and in restricted niches of the adult brain in a process called neurogenesis. The precise control of cell proliferation and differentiation in time and space required for neurogenesis depends on sophisticated orchestration of gene transcription in neural precursor cells. Much progress has been made in understanding the transcriptional regulation of neurogenesis, which relies on dose- and context-dependent expression of specific transcription factors that regulate the maintenance and proliferation of neural progenitors, followed by their differentiation into lineage-specified cells. Here, we review some of the most widely studied neurogenic transcription factors in the embryonic cortex and neurogenic niches in the adult brain. We compare functions of these transcription factors in embryonic and adult neurogenesis, highlighting biochemical, developmental, and cell biological properties. Our goal is to present an overview of transcriptional regulation underlying neurogenesis in the developing cerebral cortex and in the adult brain.
Language	English
Publishing date	2023-07-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2023.1217596
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Proteomic analysis of the developing mammalian brain links PCDH19 to the Wnt/β-catenin signalling pathway.

de Nys, Rebekah / Gardner, Alison / van Eyk, Clare / Mincheva-Tasheva, Stefka / Thomas, Paul / Bhattacharjee, Rudrarup / Jolly, Lachlan / Martinez-Garay, Isabel / Fox, Ian W J / Kamath, Karthik Shantharam / Kumar, Raman / Gecz, Jozef

Molecular psychiatry

2024

Abstract: Clustering Epilepsy (CE) is a neurological disorder caused by pathogenic variants of the Protocadherin 19 (PCDH19) gene. PCDH19 encodes a protein involved in cell adhesion and Estrogen Receptor α mediated-gene regulation. To gain further insights into ... ...

Abstract	Clustering Epilepsy (CE) is a neurological disorder caused by pathogenic variants of the Protocadherin 19 (PCDH19) gene. PCDH19 encodes a protein involved in cell adhesion and Estrogen Receptor α mediated-gene regulation. To gain further insights into the molecular role of PCDH19 in the brain, we investigated the PCDH19 interactome in the developing mouse hippocampus and cortex. Combined with a meta-analysis of all reported PCDH19 interacting proteins, our results show that PCDH19 interacts with proteins involved in actin, microtubule, and gene regulation. We report CAPZA1, αN-catenin and, importantly, β-catenin as novel PCDH19 interacting proteins. Furthermore, we show that PCDH19 is a regulator of β-catenin transcriptional activity, and that this pathway is disrupted in CE individuals. Overall, our results support the involvement of PCDH19 in the cytoskeletal network and point to signalling pathways where PCDH19 plays critical roles.
Language	English
Publishing date	2024-03-07
Publishing country	England
Document type	Journal Article
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-024-02482-z
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 4812: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Neuregulin-4 Is Required for Maintaining Soma Size of Pyramidal Neurons in the Motor Cortex.

Paramo, Blanca / Bachmann, Sven O / Baudouin, Stéphane J / Martinez-Garay, Isabel / Davies, Alun M

eNeuro

2021 Volume 8, Issue 1

Abstract: The regulation of neuronal soma size is essential for appropriate brain circuit function and its dysregulation is associated with several neurodevelopmental disorders. A defect in the dendritic growth and elaboration of motor neocortical pyramidal ... ...

Abstract	The regulation of neuronal soma size is essential for appropriate brain circuit function and its dysregulation is associated with several neurodevelopmental disorders. A defect in the dendritic growth and elaboration of motor neocortical pyramidal neurons in neonates lacking neuregulin-4 (NRG4) has previously been reported. In this study, we investigated whether the loss of NRG4 causes further morphologic defects that are specific to these neurons. We analyzed the soma size of pyramidal neurons of layer (L)2/3 and L5 of the motor cortex and a subpopulation of multipolar interneurons in this neocortical region in
MeSH term(s)	Animals ; Mice ; Mice, Knockout ; Motor Cortex/metabolism ; Neuregulins/genetics ; Neurons/cytology ; Pyramidal Cells/cytology
Chemical Substances	Neuregulins ; neuregulin-4
Language	English
Publishing date	2021-02-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0288-20.2021
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Cellular and Behavioral Characterization of

Galindo-Riera, Natalia / Newbold, Sylvia Adriana / Sledziowska, Monika / Llinares-Benadero, Cristina / Griffiths, Jessica / Mire, Erik / Martinez-Garay, Isabel

eNeuro

2021 Volume 8, Issue 4

Abstract: Mutations in the X-linked cell adhesion protein PCDH19 lead to seizures, cognitive impairment, and other behavioral comorbidities when present in a mosaic pattern. Neither the molecular mechanisms underpinning this disorder nor the function of PCDH19 ... ...

Abstract	Mutations in the X-linked cell adhesion protein PCDH19 lead to seizures, cognitive impairment, and other behavioral comorbidities when present in a mosaic pattern. Neither the molecular mechanisms underpinning this disorder nor the function of PCDH19 itself are well understood. By combining RNA
MeSH term(s)	Animals ; Cadherins/genetics ; Exploratory Behavior ; Female ; Mice ; Mutation/genetics ; Neurons ; Seizures ; Social Environment
Chemical Substances	Cadherins
Language	English
Publishing date	2021-08-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0510-20.2021
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Dbx1-Derived Pyramidal Neurons Are Generated Locally in the Developing Murine Neocortex.

Rueda-Alaña, Eneritz / Martínez-Garay, Isabel / Encinas, Juan Manuel / Molnár, Zoltán / García-Moreno, Fernando

Frontiers in neuroscience

2018 Volume 12, Page(s) 792

Abstract: The neocortex (NCx) generates at the dorsal region of the pallium in the forebrain. Several adjacent structures also contribute with neurons to NCx. Ventral pallium (VP) is considered to generate several populations of neurons that arrive through ... ...

Abstract	The neocortex (NCx) generates at the dorsal region of the pallium in the forebrain. Several adjacent structures also contribute with neurons to NCx. Ventral pallium (VP) is considered to generate several populations of neurons that arrive through tangential migration to the NCx. Amongst them are the Cajal-Retzius cells and some transient pyramidal neurons. However, the specific site and timing of generation, trajectory of migration and actual contribution to the pyramidal population remains elusive. Here, we investigate the spatio-temporal origin of neuronal populations from VP in an
Language	English
Publishing date	2018-10-31
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2018.00792
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The placenta protects the fetal circulation from anxiety-driven elevations in maternal serum levels of brain-derived neurotrophic factor.

Dingsdale, Hayley / Nan, Xinsheng / Garay, Samantha M / Mueller, Annett / Sumption, Lorna A / Chacón-Fernández, Pedro / Martinez-Garay, Isabel / Ghevaert, Cedric / Barde, Yves-Alain / John, Rosalind M

Translational psychiatry

2021 Volume 11, Issue 1, Page(s) 62

Abstract: Brain-derived neurotrophic factor (BDNF) plays crucial roles in brain function. Numerous studies report alterations in BDNF levels in human serum in various neurological conditions, including mood disorders such as depression. However, little is known ... ...

Abstract	Brain-derived neurotrophic factor (BDNF) plays crucial roles in brain function. Numerous studies report alterations in BDNF levels in human serum in various neurological conditions, including mood disorders such as depression. However, little is known about BDNF levels in the blood during pregnancy. We asked whether maternal depression and/or anxiety during pregnancy were associated with altered serum BDNF levels in mothers (n = 251) and their new-born infants (n = 212). As prenatal exposure to maternal mood disorders significantly increases the risk of neurological conditions in later life, we also examined the possibility of placental BDNF transfer by developing a new mouse model. We found no association between maternal symptoms of depression and either maternal or infant cord blood serum BDNF. However, maternal symptoms of anxiety correlated with significantly raised maternal serum BDNF exclusively in mothers of boys (r = 0.281; P = 0.005; n = 99). Serum BDNF was significantly lower in male infants than female infants but neither correlated with maternal anxiety symptoms. Consistent with this observation, we found no evidence for BDNF transfer across the placenta. We conclude that the placenta protects the developing fetus from maternal changes in serum BDNF that could otherwise have adverse consequences for fetal development.
MeSH term(s)	Anxiety ; Brain-Derived Neurotrophic Factor ; Female ; Fetal Blood ; Humans ; Male ; Placenta ; Pregnancy ; Serum
Chemical Substances	Brain-Derived Neurotrophic Factor
Language	English
Publishing date	2021-01-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-020-01176-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: The neuronal migration hypothesis of dyslexia: A critical evaluation 30 years on.

Guidi, Luiz G / Velayos-Baeza, Antonio / Martinez-Garay, Isabel / Monaco, Anthony P / Paracchini, Silvia / Bishop, Dorothy V M / Molnár, Zoltán

The European journal of neuroscience

2018 Volume 48, Issue 10, Page(s) 3212–3233

Abstract: The capacity for language is one of the key features underlying the complexity of human cognition and its evolution. However, little is known about the neurobiological mechanisms that mediate normal or impaired linguistic ability. For developmental ... ...

Abstract	The capacity for language is one of the key features underlying the complexity of human cognition and its evolution. However, little is known about the neurobiological mechanisms that mediate normal or impaired linguistic ability. For developmental dyslexia, early postmortem studies conducted in the 1980s linked the disorder to subtle defects in the migration of neurons in the developing neocortex. These early studies were reinforced by human genetic analyses that identified dyslexia susceptibility genes and subsequent evidence of their involvement in neuronal migration. In this review, we examine recent experimental evidence that does not support the link between dyslexia and neuronal migration. We critically evaluate gene function studies conducted in rodent models and draw attention to the lack of robust evidence from histopathological and imaging studies in humans. Our review suggests that the neuronal migration hypothesis of dyslexia should be reconsidered, and the neurobiological basis of dyslexia should be approached with a fresh start.
MeSH term(s)	Animals ; Cell Movement ; Disease Models, Animal ; Dyslexia/etiology ; Dyslexia/genetics ; Genetic Predisposition to Disease/genetics ; Humans ; Neocortex/cytology ; Neurons/cytology
Language	English
Publishing date	2018-10-06
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/ejn.14149
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 2548: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: VISIONS: the art of science.

Gil-Sanz, Cristina / Martinez-Garay, Isabel

Molecular reproduction and development

2010 Volume 77, Issue 3, Page(s) 195

MeSH term(s)	Animals ; Electroporation ; Embryo, Mammalian ; Integrases/genetics ; Integrases/metabolism ; Luminescent Proteins/genetics ; Luminescent Proteins/metabolism ; Microscopy, Fluorescence ; Neurons/cytology ; Neurons/metabolism ; Telencephalon/cytology ; Telencephalon/growth & development
Chemical Substances	Luminescent Proteins ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2010-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	20321-x
ISSN	1098-2795 ; 1040-452X
ISSN (online)	1098-2795
ISSN	1040-452X
DOI	10.1002/mrd.21159
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2759: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Knockout Mice for Dyslexia Susceptibility Gene Homologs KIAA0319 and KIAA0319L have Unaffected Neuronal Migration but Display Abnormal Auditory Processing.

Guidi, Luiz G / Mattley, Jane / Martinez-Garay, Isabel / Monaco, Anthony P / Linden, Jennifer F / Velayos-Baeza, Antonio / Molnár, Zoltán

Cerebral cortex (New York, N.Y. : 1991)

2017 Volume 27, Issue 12, Page(s) 5831–5845

Abstract: Developmental dyslexia is a neurodevelopmental disorder that affects reading ability caused by genetic and non-genetic factors. Amongst the susceptibility genes identified to date, KIAA0319 is a prime candidate. RNA-interference experiments in rats ... ...

Abstract	Developmental dyslexia is a neurodevelopmental disorder that affects reading ability caused by genetic and non-genetic factors. Amongst the susceptibility genes identified to date, KIAA0319 is a prime candidate. RNA-interference experiments in rats suggested its involvement in cortical migration but we could not confirm these findings in Kiaa0319-mutant mice. Given its homologous gene Kiaa0319L (AU040320) has also been proposed to play a role in neuronal migration, we interrogated whether absence of AU040320 alone or together with KIAA0319 affects migration in the developing brain. Analyses of AU040320 and double Kiaa0319;AU040320 knockouts (dKO) revealed no evidence for impaired cortical lamination, neuronal migration, neurogenesis or other anatomical abnormalities. However, dKO mice displayed an auditory deficit in a behavioral gap-in-noise detection task. In addition, recordings of click-evoked auditory brainstem responses revealed suprathreshold deficits in wave III amplitude in AU040320-KO mice, and more general deficits in dKOs. These findings suggest that absence of AU040320 disrupts firing and/or synchrony of activity in the auditory brainstem, while loss of both proteins might affect both peripheral and central auditory function. Overall, these results stand against the proposed role of KIAA0319 and AU040320 in neuronal migration and outline their relationship with deficits in the auditory system.
MeSH term(s)	Action Potentials/physiology ; Adaptation, Physiological/physiology ; Animals ; Auditory Perception/physiology ; Cell Movement/physiology ; Cerebral Cortex/growth & development ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Dyslexia/genetics ; Evoked Potentials, Auditory, Brain Stem/physiology ; Female ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Nerve Tissue Proteins/deficiency ; Nerve Tissue Proteins/genetics ; Neurogenesis/physiology ; Neurons/metabolism ; Neurons/pathology ; Receptors, Cell Surface/deficiency ; Receptors, Cell Surface/genetics
Chemical Substances	KIAA0319 protein, mouse ; KIAA0319L protein, mouse ; Nerve Tissue Proteins ; Receptors, Cell Surface
Language	English
Publishing date	2017-08-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1077450-6
ISSN	1460-2199 ; 1047-3211
ISSN (online)	1460-2199
ISSN	1047-3211
DOI	10.1093/cercor/bhx269
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3235: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito