Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex
- Argandoña, Enrike G. Department of Medicine. Unit of Anatomy. University of Fribourg, Switzerland
- Bengoetxea, Harkaitz Laboratory of Experimental Neuroscience LaNCE, Department of Neuroscience, University of the Basque Country (UPV/EHU), Leioa, Spain
- Bulnes, Susana Laboratory of Experimental Neuroscience LaNCE, Department of Neuroscience, University of the Basque Country (UPV/EHU), Leioa, Spain
- Rico-Barrio, Irantzu Laboratory of Experimental Neuroscience LaNCE, Department of Neuroscience, University of the Basque Country (UPV/EHU), Leioa, Spain
- Ortuzar, Naiara Laboratory of Experimental Neuroscience LaNCE, Department of Neuroscience, University of the Basque Country (UPV/EHU), Leioa, Spain
- Lafuente, José Vicente Laboratory of Experimental Neuroscience LaNCE, Department of Neuroscience, University of the Basque Country (UPV/EHU), Leioa, Spain
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21.07.2012
Published in:
- Brain Research. - 2012, vol. 1473, p. 141–154
English
VEGF is the major angiogenic and vascular permeability factor in health and disease. Vascular development depends on function, and in sensory areas is experience-dependent. Our aim was to investigate, qualitatively and quantitatively, the effects of intracortical infusion and neutralisation of VEGF during the first days of the critical visual period, when peak levels of endogenous VEGF secretion are reached.VEGF was intracortically delivered into middle cortical layers of P18 Long–Evans rats. Another cohort received anti-VEGF. Vehicle (PBS)-infused and non-operated animals were used as controls. Various immunopathological analyses were performed: Endothelial Barrier Antigen (EBA) for the BBB integrity and GFAP for astroglial response. Vascular density was measured by Butyryl Cholinesterase Histochemistry, neuronal density by NeuN immunohistochemistry and apoptosis by TUNEL staining. VEGF levels were measured by Western Blot.Decreased vascular permeability was evoked in VEGF-infused rats whilst EBA expression remained constant, suggesting a preserved BBB function. When VEGF was blocked, tissue showed a higher degree of extravasation and a decreased number of EBA-positive vessels surrounding the injury. Lesion induced by cannula implantation annulled the normal increase in vascular density and the decrease in neuronal density during this time. VEGF rescued in part the vascular increase, and also prevented physiological and pathological neuronal death. VEGF blockade induced a higher amount of neural loss and lower astrocytic reaction.Our results support the role of VEGF as extending beyond vascularization, preventing physiological and pathological neuronal death, not only in the injured hemisphere but also in the intact one suggesting a process of transhemispheric diaschisis.
- Faculty
- Faculté des sciences et de médecine
- Department
- Département de Médecine
- Language
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- English
- Classification
- Biological sciences
- License
- License undefined
- Identifiers
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- RERO DOC 29730
- DOI 10.1016/j.brainres.2012.07.008
- Persistent URL
- https://folia.unifr.ch/unifr/documents/302554
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