Search

Your search keyword '"Neonatal excitotoxicity"' showing total 3 results
Start Over Descriptor "Neonatal excitotoxicity"
3 results on '"Neonatal excitotoxicity"'

1. Neonatal hypoxic preconditioning involves vascular endothelial growth factor

Author

Vincent Laudenbach, Romain H. Fontaine, Fadia Medja, Peter Carmeliet, Daniel J. Hicklin, Jorge Gallego, Philippe Leroux, Stéphane Marret, and Pierre Gressens

Subjects
Neonatal excitotoxicity, NMDA receptors, Ibotenate, AMPA-kainate receptors, S-willardiine, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

We studied hypoxic preconditioning (HxP) in the murine developing brain, focusing on the role for vascular endothelial growth factor (VEGF). Newborn mice were used as follows: (1) HxP (or normoxia) then intracerebral (i.c.) NMDA or AMPA-kainate agonist; (2) HxP then intraperitoneal (i.p.) anti-VEGFR2/Flk1 or anti-VEGFR1/Flt1 monoclonal blocking antibody (mAb) then i.c. NMDA/AMPA-kainate agonist; (3) i.p. VEGF then i.c. NMDA/AMPA-kainate agonist; and (4) in mutants lacking the hypoxia-responsive element (HRE) of the VEGF-A gene (VEGF∂/∂) and their wild-type littermates (VEGF+/+), HxP followed by i.c. NMDA agonist.HxP reduced the size of NMDA-related cortical and AMPA-kainate-related cortical and white matter excitotoxic lesions. Anti-VEGFR2/Flk1 mAb prevented HxP-induced neuroprotection. VEGF produced dose-dependent reduction in cortical lesions. HxP did not prevent, but instead exacerbated, brain lesions in VEGF∂/∂ mutants. Thus, exogenous as well as endogenous VEGF reduces excitotoxic brain lesions in the developing mouse. The VEGF/VEGFR2/Flk1 pathway is involved in the neuroprotective response to HxP.

Published
2007
Full Text
View/download PDF

2. Neonatal hypoxic preconditioning involves vascular endothelial growth factor

Author

Laudenbach, Vincent, Fontaine, Romain H., Medja, Fadia, Carmeliet, Peter, Hicklin, Daniel J., Gallego, Jorge, Leroux, Philippe, Marret, Stéphane, and Gressens, Pierre

Subjects
*VASCULAR endothelial growth factors, *MICE, *PRECANCEROUS conditions, *IMMUNOREGULATION
Abstract

Abstract: We studied hypoxic preconditioning (HxP) in the murine developing brain, focusing on the role for vascular endothelial growth factor (VEGF). Newborn mice were used as follows: (1) HxP (or normoxia) then intracerebral (i.c.) NMDA or AMPA-kainate agonist; (2) HxP then intraperitoneal (i.p.) anti-VEGFR2/Flk1 or anti-VEGFR1/Flt1 monoclonal blocking antibody (mAb) then i.c. NMDA/AMPA-kainate agonist; (3) i.p. VEGF then i.c. NMDA/AMPA-kainate agonist; and (4) in mutants lacking the hypoxia-responsive element (HRE) of the VEGF-A gene (VEGF ∂/∂ ) and their wild-type littermates (VEGF +/+ ), HxP followed by i.c. NMDA agonist. HxP reduced the size of NMDA-related cortical and AMPA-kainate-related cortical and white matter excitotoxic lesions. Anti-VEGFR2/Flk1 mAb prevented HxP-induced neuroprotection. VEGF produced dose-dependent reduction in cortical lesions. HxP did not prevent, but instead exacerbated, brain lesions in VEGF ∂/∂ mutants. Thus, exogenous as well as endogenous VEGF reduces excitotoxic brain lesions in the developing mouse. The VEGF/VEGFR2/Flk1 pathway is involved in the neuroprotective response to HxP. [Copyright &y& Elsevier]

Published
2007
Full Text
View/download PDF

3. Neonatal hypoxic preconditioning involves vascular endothelial growth factor

Author

Daniel J. Hicklin, Fadia Medja, Jorge Gallego, Peter Carmeliet, Romain H. Fontaine, Philippe Leroux, Stéphane Marret, Vincent Laudenbach, and Pierre Gressens

Subjects
Vascular Endothelial Growth Factor A, Agonist, Aging, medicine.medical_specialty, S-willardiine, medicine.drug_class, Mice, Transgenic, Pyrimidinones, AMPA receptor, Biology, NMDA receptors, Neuroprotection, lcsh:RC321-571, AMPA-kainate receptors, Mice, chemistry.chemical_compound, Internal medicine, Weight Loss, Excitatory Amino Acid Agonists, medicine, Animals, Neonatal excitotoxicity, Antibodies, Blocking, Hypoxia, Brain, Promoter Regions, Genetic, Uracil, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, Ibotenic Acid, Alanine, Vascular Endothelial Growth Factor Receptor-1, Brain, Kinase insert domain receptor, Vascular Endothelial Growth Factor Receptor-2, Recombinant Proteins, Ibotenate, Vascular endothelial growth factor, Vascular endothelial growth factor A, Endocrinology, Animals, Newborn, nervous system, Neurology, chemistry, Mutation, NMDA receptor, Injections, Intraperitoneal, Ibotenic acid
Abstract

We studied hypoxic preconditioning (HxP) in the murine developing brain, focusing on the role for vascular endothelial growth factor (VEGF). Newborn mice were used as follows: (1) HxP (or normoxia) then intracerebral (i.c.) NMDA or AMPA-kainate agonist; (2) HxP then intraperitoneal (i.p.) anti-VEGFR2/Flk1 or anti-VEGFR1/Flt1 monoclonal blocking antibody (mAb) then i.c. NMDA/AMPA-kainate agonist; (3) i.p. VEGF then i.c. NMDA/AMPA-kainate agonist; and (4) in mutants lacking the hypoxia-responsive element (HRE) of the VEGF-A gene (VEGF( partial differential/ partial differential)) and their wild-type littermates (VEGF(+/+)), HxP followed by i.c. NMDA agonist. HxP reduced the size of NMDA-related cortical and AMPA-kainate-related cortical and white matter excitotoxic lesions. Anti-VEGFR2/Flk1 mAb prevented HxP-induced neuroprotection. VEGF produced dose-dependent reduction in cortical lesions. HxP did not prevent, but instead exacerbated, brain lesions in VEGF( partial differential/ partial differential) mutants. Thus, exogenous as well as endogenous VEGF reduces excitotoxic brain lesions in the developing mouse. The VEGF/VEGFR2/Flk1 pathway is involved in the neuroprotective response to HxP.

Published
2007

Catalog

Books, media, physical & digital resources
See catalog results