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Your search keyword '"Yves-Alain Barde"' showing total 3 results
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3 results on '"Yves-Alain Barde"'

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

Author

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

Subjects
Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

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.

Published
2021
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2. Neurotrophin receptors TrkA and TrkC cause neuronal death whereas TrkB does not

Author

Miriam Bibel, Vassiliki Nikoletopoulou, Chantal Rencurel, Lixin Zhang, Yves-Alain Barde, José María Frade, Heiko Lickert, and Patrizia Giallonardo

Subjects
animal structures, Molecular biology, Tropomyosin receptor kinase B, Stem cells, Biology, Tropomyosin receptor kinase A, Tropomyosin receptor kinase C, Mice, Developmental biology, medicine, Low-affinity nerve growth factor receptor, Animals, Receptor, trkB, Receptor, trkC, Receptor, trkA, Embryonic Stem Cells, Neurons, Multidisciplinary, Cell Death, Cell Differentiation, Sensory neuron, Cell biology, Autonomic nervous system, medicine.anatomical_structure, nervous system, Trk receptor, Immunology, biology.protein, Neurotrophin, Neuroscience
Abstract

12 páginas, Neurons of the peripheral nervous system have long been known to require survival factors to prevent their death during development. But why they selectively become dependent on secretory molecules has remained a mystery, as is the observation that in the central nervous system, most neurons do not show this dependency. Using engineered embryonic stem cells, we show here that the neurotrophin receptors TrkA and TrkC (tropomyosin receptor kinase A and C, also known as Ntrk1 and Ntrk3, respectively) instruct developing neurons to die, both in vitro and in vivo. By contrast, TrkB (also known as Ntrk2), a closely related receptor primarily expressed in the central nervous system, does not. These results indicate that TrkA and TrkC behave as dependence receptors, explaining why developing sympathetic and sensory neurons become trophic-factor-dependent for survival. We suggest that the expansion of the Trk gene family that accompanied the segregation of the peripheral from the central nervous system generated a novel mechanism of cell number control, H.L. is supported by an Emmy-Nother fellowship of the DFG.

Published
2010

3. The zinc finger protein NRIF interacts with the neurotrophin receptor p75(NTR) and participates in programmed cell death

Author

Georg Dechant, Yves-Alain Barde, Isabel Benzel, Elisabeth Casademunt, José María Frade, and Bruce D. Carter

Subjects
Genetically modified mouse, Programmed cell death, Recombinant Fusion Proteins, Molecular Sequence Data, Kruppel-Like Transcription Factors, Apoptosis, Transfection, Receptor, Nerve Growth Factor, General Biochemistry, Genetics and Molecular Biology, Retina, Finger protein, Cell Line, Embryonic and Fetal Development, Mice, Krüppel, 75NTRzinc, Animals, Amino Acid Sequence, RNA, Messenger, Cloning, Molecular, Receptor, Molecular Biology, Genetic backgroundp, Zinc finger, Mice, Knockout, Binding Sites, General Immunology and Microbiology, biology, General Neuroscience, Intracellular Signaling Peptides and Proteins, Gene targeting, Zinc Fingers, Molecular biology, Cell biology, DNA-Binding Proteins, Repressor Proteins, Embryonic lethality, nervous system, Gene Targeting, biology.protein, sense organs, Carrier Proteins, Neurotrophin, Protein Binding, Transcription Factors, Research Article
Abstract

NRIF (neurotrophin receptor interacting factor) is a ubiquitously expressed zinc finger protein of the Kruppel family which interacts with the neurotrophin receptor p75(NTR). The interaction was first detected in yeast and then biochemically confirmed using recombinant GST-NRIF fusions and p75(NTR) expressed by eukaryotic cells. Transgenic mice carrying a deletion in the exon encoding the p75(NTR)-binding domain of NRIF display a phenotype which is strongly dependent upon genetic background. While at the F2 generation there is only limited (20%) embryonic lethality, in a congenic BL6 strain nrif(-/-) mice cannot survive beyond E12, but are viable and healthy to adulthood in the Sv129 background. The involvement of NRIF in p75(NTR)/NGF-mediated developmental cell death was examined in the mouse embryonic neural retina. Disruption of the nrif gene leads to a reduction in cell death which is quantitatively indistinguishable from that observed in p75(NTR-/-) and ngf(-/-) mice. These results indicate that NRIF is an intracellular p75(NTR)-binding protein transducing cell death signals during development.

Published
1999

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