Absence of striatal newborn neurons with mature phenotype following defined striatal and cortical excitotoxic brain injuries.
Deierborg, Tomas LU ; Staflin, Karin LU ; Pesic, Jelena ; Roybon, Laurent LU ; Brundin, Patrik LU and Lundberg, Cecilia LU
(2009)
In Experimental Neurology
219.
p.363-367
- Abstract
- Experimental stroke and excitotoxic brain lesion to the striatum or cortex increase the proliferation of cells residing within the ventricular wall and cause subsequent migration of newborn neuroblasts into the lesioned brain parenchyma. In this study, we clarify the different events of neurogenesis following striatal or cortical excitotoxic brain lesions in adult rats. Newborn cells were labeled by intraperitoneal injection of bromo-deoxy-uridine (BrdU), or by green fluorescent protein (GFP)-expressing lentiviral vectors injected into the subventricular zone (SVZ). We show that only neural progenitors born the first 5 days in the SVZ reside and expand within this neurogenic niche over time, and that these early labeled cells are more... (More)
- Experimental stroke and excitotoxic brain lesion to the striatum or cortex increase the proliferation of cells residing within the ventricular wall and cause subsequent migration of newborn neuroblasts into the lesioned brain parenchyma. In this study, we clarify the different events of neurogenesis following striatal or cortical excitotoxic brain lesions in adult rats. Newborn cells were labeled by intraperitoneal injection of bromo-deoxy-uridine (BrdU), or by green fluorescent protein (GFP)-expressing lentiviral vectors injected into the subventricular zone (SVZ). We show that only neural progenitors born the first 5 days in the SVZ reside and expand within this neurogenic niche over time, and that these early labeled cells are more prone to migrate towards the striatum as neuroblasts. However, these neuroblasts could not mature into NeuN(+) neurons in the striatum. Furthermore, we found that cortical lesions, close or distant from the SVZ, could not upregulate SVZ cell proliferation nor promote neurogenesis. Our study demonstrates that both the time window for labeling proliferating cells and the site of lesion are crucial when assessing neurogenesis following brain injury. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1412520
- author
- Deierborg, Tomas
LU
; Staflin, Karin
LU
; Pesic, Jelena
; Roybon, Laurent
LU
; Brundin, Patrik
LU
and Lundberg, Cecilia
LU
- organization
- publishing date
- 2009
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Experimental Neurology
- volume
- 219
- pages
- 363 - 367
- publisher
- Elsevier
- external identifiers
-
- wos:000269398600043
- pmid:19427853
- scopus:68749099422
- pmid:19427853
- ISSN
- 0014-4886
- DOI
- 10.1016/j.expneurol.2009.05.002
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: CNS Gene Therapy (013212029), Neuronal Survival (013212041)
- id
- 683a6ca5-b32f-4758-9bd2-e247f7361ea1 (old id 1412520)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/19427853?dopt=Abstract
- date added to LUP
- 2016-04-04 08:54:33
- date last changed
- 2022-01-29 07:34:16
@article{683a6ca5-b32f-4758-9bd2-e247f7361ea1,
abstract = {{Experimental stroke and excitotoxic brain lesion to the striatum or cortex increase the proliferation of cells residing within the ventricular wall and cause subsequent migration of newborn neuroblasts into the lesioned brain parenchyma. In this study, we clarify the different events of neurogenesis following striatal or cortical excitotoxic brain lesions in adult rats. Newborn cells were labeled by intraperitoneal injection of bromo-deoxy-uridine (BrdU), or by green fluorescent protein (GFP)-expressing lentiviral vectors injected into the subventricular zone (SVZ). We show that only neural progenitors born the first 5 days in the SVZ reside and expand within this neurogenic niche over time, and that these early labeled cells are more prone to migrate towards the striatum as neuroblasts. However, these neuroblasts could not mature into NeuN(+) neurons in the striatum. Furthermore, we found that cortical lesions, close or distant from the SVZ, could not upregulate SVZ cell proliferation nor promote neurogenesis. Our study demonstrates that both the time window for labeling proliferating cells and the site of lesion are crucial when assessing neurogenesis following brain injury.}},
author = {{Deierborg, Tomas and Staflin, Karin and Pesic, Jelena and Roybon, Laurent and Brundin, Patrik and Lundberg, Cecilia}},
issn = {{0014-4886}},
language = {{eng}},
pages = {{363--367}},
publisher = {{Elsevier}},
series = {{Experimental Neurology}},
title = {{Absence of striatal newborn neurons with mature phenotype following defined striatal and cortical excitotoxic brain injuries.}},
url = {{http://dx.doi.org/10.1016/j.expneurol.2009.05.002}},
doi = {{10.1016/j.expneurol.2009.05.002}},
volume = {{219}},
year = {{2009}},
}