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Dopaminergic lesion enhances growth factor-induced striatal neuroblast migration.

Journal article
Authors Beate Winner
Sebastien Couillard-Despres
Martin Geyer
Robert Aigner
Ulrich Bogdahn
Ludwig Aigner
Hans-Georg Kuhn
Jürgen Winkler
Published in Journal of neuropathology and experimental neurology
Volume 67
Issue 2
Pages 105-16
ISSN 0022-3069
Publication year 2008
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Pages 105-16
Language en
Links dx.doi.org/10.1097/nen.0b013e318163...
Keywords Animals, Brain Injuries, chemically induced, drug therapy, pathology, physiopathology, Cell Count, Cell Differentiation, drug effects, Cell Movement, drug effects, physiology, Cell Proliferation, drug effects, Corpus Striatum, drug effects, pathology, Disease Models, Animal, Dopamine, metabolism, Female, In Situ Nick-End Labeling, Intercellular Signaling Peptides and Proteins, administration & dosage, Nerve Tissue Proteins, metabolism, Neurons, drug effects, physiology, Oxidopamine, Rats, Rats, Wistar
Subject categories Neuroscience

Abstract

Adult neurogenesis persists in the subventricular zone and is decreased in Parkinson disease (PD). The therapeutic potential of neurogenesis in PD requires understanding of mechanisms of 1) neural stem cell generation; 2) their guidance to the lesion site; and 3) the environment that enables neuronal differentiation, survival, and functional integration. We examined the combined intraventricular infusion of epidermal growth factor (EGF) and fibroblast growth factor 2 (FGF-2) in a 6-hydroxydopamine-induced rodent model of PD. Epidermal growth factor and FGF-2 induced a massive increase in cell proliferation and in numbers of doublecortin-expressing neuroblasts in the subventricular zone. These growth factors also increased dopaminergic neurogenesis in the olfactory bulb and promoted the migration of newly generated neuroblasts from the subventricular zone into the adjacent striatum. The effects of EGF and FGF-2 were present in unlesioned animals but were dramatically enhanced in 6-hydroxydopamine-lesioned animals.These findings suggest that newly generated neuroblasts may be redirected to the region of dopaminergic deficit, and that EGF and FGF-2 can enhance dopaminergic neurogenesis in the olfactory bulb but not in the striatum. Similar mechanisms may be involved in the increased numbers of dopaminergic neurons observed in the olfactory bulbs of PD patients and their functional olfactory deficits.

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