Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex

Argandoña, Enrike; Bengoetxea, Harkaitz; Bulnes, Susana; Rico‐Barrio, Irantzu; Ortuzar, Naiara; Lafuente, José Vicente

doi:10.1016/j.brainres.2012.07.008

Cited by 5 publications

(4 citation statements)

References 93 publications

(108 reference statements)

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“…Why supplementing diabetic mice with VEGF, which is often thought to induce angiogenesis and BBB disruption in certain conditions such as stroke (Ma et al, 2012;Reeson et al, 2015), would normalize vessel density/width, prevent BBB disruption and spine loss in our experiments is not entirely clear. However, there has been a report showing that VEGF infusion can reduce lesion induced BBB permeability in juvenile rat cortex (Argandona et al, 2012). Furthermore, since constitutive VEGF-R2 signaling is thought to play an important role in maintaining vascular homeostasis and can act as a negative regulator of trans-cytotic machinery proteins such as Caveolin-1 (Liu et al, 1999), it is possible that our VEGF treatment simply restored VEGF signaling to a level that is required for maintaining ongoing endothelial cell function/structure and normal trans-endothelial transport.…”

Section: Discussionmentioning

confidence: 93%

VEGF can protect against blood brain barrier dysfunction, dendritic spine loss and spatial memory impairment in an experimental model of diabetes

Taylor¹,

Trudeau²,

Arnold³

et al. 2015

Neurobiology of Disease

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Section: Discussionmentioning

confidence: 93%

VEGF can protect against blood brain barrier dysfunction, dendritic spine loss and spatial memory impairment in an experimental model of diabetes

Taylor¹,

Trudeau²,

Arnold³

et al. 2015

Neurobiology of Disease

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“…Unal-Cevik et al ( 2004 ) found that a significant number of neurons lose their NeuN positivity after cerebral ischemia, but preserve their integrity. In another study loss of NeuN staining was an early marker of injured, but still rescuable cortical neurons (Argandoña et al, 2012 ). In our study restraint stress did not cause change in neuronal cell density in the frontal cortex and in the CA1 region of hippocampus, while a trend for a decreased density was observed in the dentate gyrus of hippocampus, which is particularly sensitive to stress (Zitman and Richter-Levin, 2013 ).…”

Section: Discussionmentioning

confidence: 98%

“…NeuN is a soluble nuclear protein and a marker for mature neurons the expression of which is sensitive to injury (Unal-Cevik et al, 2004 ; Argandoña et al, 2012 ). Unal-Cevik et al ( 2004 ) found that a significant number of neurons lose their NeuN positivity after cerebral ischemia, but preserve their integrity.…”

Section: Discussionmentioning

confidence: 99%

Restraint Stress-Induced Morphological Changes at the Blood-Brain Barrier in Adult Rats

Sántha

Veszelka

Hoyk

et al. 2016

Front. Mol. Neurosci.

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Stress is well-known to contribute to the development of both neurological and psychiatric diseases. While the role of the blood-brain barrier is increasingly recognized in the development of neurodegenerative disorders, such as Alzheimer's disease, dysfunction of the blood-brain barrier has been linked to stress-related psychiatric diseases only recently. In the present study the effects of restraint stress with different duration (1, 3, and 21 days) were investigated on the morphology of the blood-brain barrier in male adult Wistar rats. Frontal cortex and hippocampus sections were immunostained for markers of brain endothelial cells (claudin-5, occluding, and glucose transporter-1) and astroglia (GFAP). Staining pattern and intensity were visualized by confocal microscopy and evaluated by several types of image analysis. The ultrastructure of brain capillaries was investigated by electron microscopy. Morphological changes and intensity alterations in brain endothelial tight junction proteins claudin-5 and occludin were induced by stress. Following restraint stress significant increases in the fluorescence intensity of glucose transporter-1 were detected in brain endothelial cells in the frontal cortex and hippocampus. Significant reductions in GFAP fluorescence intensity were observed in the frontal cortex in all stress groups. As observed by electron microscopy, 1-day acute stress induced morphological changes indicating damage in capillary endothelial cells in both brain regions. After 21 days of stress thicker and irregular capillary basal membranes in the hippocampus and edema in astrocytes in both regions were seen. These findings indicate that stress exerts time-dependent changes in the staining pattern of tight junction proteins occludin, claudin-5, and glucose transporter-1 at the level of brain capillaries and in the ultrastructure of brain endothelial cells and astroglial endfeet, which may contribute to neurodegenerative processes, cognitive and behavioral dysfunctions.

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“…As in the dentate gyrus, no effect of VEGF administration was observed in the neuronal and vascular densities of the primary visual cortex in standard conditions. Previous studies in our group demonstrated that minipump implantation produced negative effects in the V1 cortex that were reverted after 1 week of VEGF administration [48,49]. In this case, we carried out a chronic VEGF or vehicle administration and therefore a chronic minipump implantation during four weeks.…”

Section: Dg-v1 Cortex Connectionmentioning

confidence: 94%

VEGF reverts the cognitive impairment induced by a focal traumatic brain injury during the development of rats raised under environmental enrichment

Ortuzar

Rico‐Barrio

Bengoetxea

et al. 2013

Behavioural Brain Research

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The role of VEGF in the nervous system is extensive; apart from its angiogenic effect, VEGF has been described as a neuroprotective, neurotrophic and neurogenic molecule. Similar effects have been described for enriched environment (EE). Moreover, both VEGF and EE have been related to improved spatial memory. Our aim was to investigate the neurovascular and cognitive effects of intracerebrallyadministered VEGF and enriched environment during the critical period of the rat visual cortex development. Results showed that VEGF infusion as well as enriched environment induced neurovascular and cognitive effects in developing rats. VEGF administration produced an enhancement during the learning process of enriched animals and acted as an angiogenic factor both in primary visual cortex (V1) and dentate gyrus (DG) in order to counteract minipump implantation-induced damage. This fact revealed that DG vascularization is critical for normal learning. In contrast to this enriched environment acted on the neuronal density of the DG and V1 cortex, and results showed learning enhancement only in non-operated rats. In conclusion, VEGF administration only has effects if damage is observed due to injury. Once control values were reached, no further effects appeared, showing a ceiling effect. Our results strongly support that in addition to neurogenesis, vascularization plays a pivotal role for learning and memory.

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Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex

Cited by 5 publications

References 93 publications

VEGF can protect against blood brain barrier dysfunction, dendritic spine loss and spatial memory impairment in an experimental model of diabetes

VEGF can protect against blood brain barrier dysfunction, dendritic spine loss and spatial memory impairment in an experimental model of diabetes

Restraint Stress-Induced Morphological Changes at the Blood-Brain Barrier in Adult Rats

VEGF reverts the cognitive impairment induced by a focal traumatic brain injury during the development of rats raised under environmental enrichment

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