Blood-brain Barrier Disruption Induces in Vivo Degeneration of Nigral Dopaminergic Neurons.
From: Departamento de Bioquímica, Bromatología, Toxicología y Medicina Legal. Facultad de Farmacia, Universidad de Sevilla, C/Prof. García González, Sevilla, Spain.
Journal of neurochemistry
- Publish Date: Jun 2007
- ISSN: 0022-3042
- Volume: 101
- Issue: 6
- Pages: 1567-82
- Medium: Print
- Language: English
- Citation (JAMA): Rite Inmaculada, Machado Alberto, Cano Josefina, et al. Blood-brain Barrier Disruption Induces in Vivo Degeneration of Nigral Dopaminergic Neurons.. J. Neurochem. Jun 2007;101:1567-82
Abstract
We have evaluated the possibility that changes in the vascular system may constitute a contributing factor for the death of nigral dopaminergic neurons in Parkinson’s disease. Thus, we have employed intranigral injections of vascular endothelial growth factor (VEGF), the most potent inducer of blood-brain barrier (BBB) permeability. A single dose of 1 mug of VEGF, chosen from a dose-response study, highly disrupted the BBB in the ventral mesencephalon in a time-dependent manner. A strong regional correlation between BBB disruption and loss of tyrosine hydroxylase-positive neurons was evident. Moreover, Fluoro-Jade B labelling showed the presence of dying neurons in the substantia nigra in response to VEGF injection. High number of TUNEL-positive nuclei was observed in this area along with activation of caspase 3 within nigral dopaminergic neurons. Analysis of the glial population demonstrated a strong inflammatory response and activation of astroglia in response to BBB disruption. We conclude that disruption of the BBB may be a causative factor for degeneration of nigral dopaminergic neurons.
Mesh Headings (Keywords): Animals, Apoptosis, Astrocytes, Blood-Brain Barrier, Dopamine, Hippocampus, Male, Microglia, Nerve Degeneration, Rats, Rats, Wistar, Substantia Nigra, Tyrosine 3-Monooxygenase, Vascular Endothelial Growth Factor A, gamma-Aminobutyric Acid
Check for Full Text / PubMed Unique Identifier (PMID): 17437543
This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.
Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.
The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.