Rat forebrain neurogenesis and striatal neuron replacement after focal stroke

The persistence of neurogenesis in the forebrain subventricular zone (SVZ) of adult mammals suggests that the mature brain maintains the potential for neuronal replacement after injury. We examined whether focal ischemic injury in adult rat would increase SVZ neurogenesis and direct migration and ne...

Full description

Saved in:
Bibliographic Details
Published in:Annals of neurology 2002-12, Vol.52 (6), p.802-813
Main Authors: Parent, Jack M., Vexler, Zinaida S., Gong, Chao, Derugin, Nikita, Ferriero, Donna M.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cell Division - physiology
Corpus Striatum - cytology
Corpus Striatum - pathology
Male
Medical sciences
Neurology
Neurons - cytology
Neurons - pathology
Prosencephalon - cytology
Prosencephalon - pathology
Rats
Rats, Sprague-Dawley
Stroke - pathology
Vascular diseases and vascular malformations of the nervous system
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The persistence of neurogenesis in the forebrain subventricular zone (SVZ) of adult mammals suggests that the mature brain maintains the potential for neuronal replacement after injury. We examined whether focal ischemic injury in adult rat would increase SVZ neurogenesis and direct migration and neuronal differentiation of endogenous precursors in damaged regions. Focal stroke was induced in adult rats by 90‐minute right middle cerebral artery occlusion (tMCAO). Cell proliferation and neurogenesis were assessed with bromodeoxyuridine (BrdU) labeling and immunostaining for cell type‐specific markers. Brains examined 10–21 days after stroke showed markedly increased SVZ neurogenesis and chains of neuroblasts extending from the SVZ to the peri‐infarct striatum. Many BrdU‐labeled cells persisted in the striatum and cortex adjacent to infarcts, but at 35 days after tMCAO only BrdU‐labeled cells in the neostriatum expressed neuronal markers. Newly generated cells in the injured neostriatum expressed markers of medium spiny neurons, which characterize most neostriatal neurons lost after tMCAO. These findings indicate that focal ischemic injury increases SVZ neurogenesis and directs neuroblast migration to sites of damage. Moreover, neuroblasts in the injured neostriatum appear to differentiate into a region‐appropriate phenotype, which suggests that the mature brain is capable of replacing some neurons lost after ischemic injury.
ISSN:0364-5134
1531-8249
DOI:10.1002/ana.10393