Cerebral ischemia and CNS transplantation: differential effects of graftedfetal rat striatal cells and human neurons derived from a clonal cell line

Citation
Cv. Borlongan et al., Cerebral ischemia and CNS transplantation: differential effects of graftedfetal rat striatal cells and human neurons derived from a clonal cell line, NEUROREPORT, 9(16), 1998, pp. 3703-3709
Citations number
30
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROREPORT
ISSN journal
09594965 → ACNP
Volume
9
Issue
16
Year of publication
1998
Pages
3703 - 3709
Database
ISI
SICI code
0959-4965(19981116)9:16<3703:CIACTD>2.0.ZU;2-Q
Abstract
STROKE mortality has declined over recent decades, prompting a demand for t he development of effective rehabilitative therapies for stroke survivors. This effort has been facilitated by significant progress in replicating the behavioral and neuropathological changes of authentic human cerebral ische mia using relevant animal models. Since the rodent model of middle cerebral artery occlusion mimics several motor abnormalities seen in clinical cereb ral ischemia, we have utilized this model to investigate treatment strategi es for stroke. The present study explored the potential benefits of neural transplantation of fetal rat striatal cells or human neurons derived from a clonal embryonal carcinoma cell line to correct the abnormalities associat ed with cerebral ischemia. We report here that ischemia-induced behavioral dysfunctions were ameliorated by the neural grafts as early as I month post -transplantation. Of note, transplantation of human neurons induced a signi ficantly more robust recovery than fetal rat striatal grafts. Thus, the log istical and ethical concerns about the use of fetal striatal cells for tran splantation therapy can be eliminated by exploiting cell line-derived human neurons as alternative graft sources. Transplantation of human neurons has a therapeutic potential for treatment of behavioral deficits associated wi th cerebral ischemia. NeuroReport 9: 3703-3709 (C) 1998 Lippincott Williams & Wilkins.