Quantitative analysis of the generation of different striatal neuronal subtypes in the adult brain following excitotoxic injury

Collin, Tove; Arvidsson, Åke; Kokaia, Zaal; Lindvall, Olle

doi:10.1016/j.expneurol.2005.03.017

Cited by 78 publications

(60 citation statements)

References 22 publications

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“…The expression of DCX, a marker for migrating neuronal progenitors, is an indication of neurogenesis as in the adult brain, within areas of continuous neurogenesis (Brown et al, 2003), or in case of increase in brain neurogenesis induced by environmental factors or insults (Couillard-Despres et al, 2005). Such an increase in neurogenesis following QA injection is in line with previous findings (Tattersfield et al, 2004;Collin et al, 2005). Our data thus support the view that SCF is produced, at least in part, by neural progenitors that migrate from the dorsal subventricular zone.…”

Section: Discussionsupporting

confidence: 90%

Stem cell factor and mesenchymal and neural stem cell transplantation in a rat model of Huntington's disease

Bantubungi

Blum

Cuvelier

et al. 2008

Molecular and Cellular Neuroscience

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Neural and mesenchymal stem cells have been proposed as alternative sources of cells for transplantation into the brain in neurodegenerative disorders. However, the endogenous factors controlling their engraftment within the injured parenchyma remain ill-defined. Here, we demonstrate significant engraftment of undifferentiated exogenous mesenchymal or neural stem cells throughout the lesioned area in a rat model for Huntington's disease, as late as 8 weeks post-transplantation. We show that stem cell factor (SCF), strongly up-regulated within host cells in the damaged striatum, is able to activate the SCF receptor c-kit and its signaling pathway and to promote the migration and proliferation of mesenchymal and neural stem cells in vitro. Furthermore, c-kit receptor blockade alters neural stem cell distribution within the lesioned striatum. Host SCF expression is observed in atypical cells expressing glial fibrillary acidic protein and doublecortin in the lesioned striatum and in migrating doublecortin-positive progenitors. Taken together, these data demonstrate that SCF produced in situ in the lesioned striatum is an important factor in promoting the engraftment of stem cells within the lesioned brain.

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Section: Discussionsupporting

confidence: 90%

Stem cell factor and mesenchymal and neural stem cell transplantation in a rat model of Huntington's disease

Bantubungi

Blum

Cuvelier

et al. 2008

Molecular and Cellular Neuroscience

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“…Studies examining progressive neurodegenerative diseases and models of Parkinson's, Huntington's, and Alzheimer's diseases have indicated that SVZ-derived NPCs can be activated and mobilized, although to a limited degree, to the site of damage [66][67][68][69][70][71], as also reported for stroke and traumatic brain injury. Ischemic stroke induced neurogenesis in the rodent SVZ [1,72,73] and stimulated newborn precursor migration to the peri-infarct regions [74,75].…”

Section: Regulation Of Npc Migration To Sites Of Neural Damagementioning

confidence: 80%

The Rho Kinase Pathway Regulates Mouse Adult Neural Precursor Cell Migration

et al. 2011

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Adult neural precursor cells (NPCs) in the subventricular zone (SVZ) normally migrate via the rostral migratory stream (RMS) to the olfactory bulb (OB). Following neural injury, they also migrate to the site of damage. This study investigated the role of Rho-dependent kinase (ROCK) on the migration of NPCs in vitro and in vivo. In vitro, using neurospheres or SVZ explants, inhibition of ROCK using Y27632 promoted cell body elongation, process protrusion, and migration, while inhibiting NPC chain formation. It had no effect on proliferation, apoptosis, or differentiation. Both isoforms of ROCK were involved. Using siRNA, knockdown of both ROCK1 and ROCK2 was required to promote NPC migration and morphological changes; knockdown of ROCK2 alone was partially effective, with little/no effect of knockdown of ROCK1 alone. In vivo, infusion of Y27632 plus Bromodeoxyuridine (BrdU) into the lateral ventricle for 1 week reduced the number of BrdU-labeled NPCs in the OB compared with BrdU infusion alone. However, ROCK inhibition did not affect the tangential-to-radial switch of NPC migration, as labeled cells were present in all OB layers. The decrease in NPC number at the OB was not attributed to a decrease in NPCs at the SVZ. However, ROCK inhibition decreased the density of BrdU-labeled cells in the RMS and increased the distribution of these cells to ectopic brain regions, such as the accessory olfactory nucleus, where the majority differentiated into neurons. These findings suggest that ROCK signaling regulates NPC migration via regulation of cell-cell contact and chain migration.

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“…This alteration in progenitor cell morphology may be in response to changes in environmental cues present in the lesioned striatum. Following recruitment into the QA-lesioned striatum, about 80% of adult-born neurons survive up to 6 weeks, when they express the mature neuronal marker NeuN and phenotypic markers of striatal medium spiny neurons (DARPP-32) and interneurons (parvalbumin or neuropeptide Y) (Tattersfield, et al, 2004, Collin, et al, 2005. However, similar to the observations made in models of ischemic stroke, relatively few adult-born neurons survive long term.…”

Section: Excitotoxic Brain Injurymentioning

confidence: 62%

“…This model has been used to investigate the effect of excitotoxic striatal injury on SVZ-derived neurogenesis. QA lesioning results in a significant increase in progenitor cell proliferation at days 1 -14 following injury (Tattersfield, et al, 2004, Collin, et al, 2005. In addition, both expansion of the RMS and aberrant migration of SVZ-derived Dcx-expressing progenitor cells into the lesioned striatum has been demonstrated following QA-induced striatum cell loss (Tattersfield, et al, 2004, Collin, et al, 2005, Gordon, et al, 2007.…”

Section: Excitotoxic Brain Injurymentioning

confidence: 99%

“…QA lesioning results in a significant increase in progenitor cell proliferation at days 1 -14 following injury (Tattersfield, et al, 2004, Collin, et al, 2005. In addition, both expansion of the RMS and aberrant migration of SVZ-derived Dcx-expressing progenitor cells into the lesioned striatum has been demonstrated following QA-induced striatum cell loss (Tattersfield, et al, 2004, Collin, et al, 2005, Gordon, et al, 2007. In order to elucidate the temporal profile of progenitor cell migration in response to QA-induced striatal cell loss, Gordon and colleagues (Gordon, et al, 2007) used retroviral tracing to label SVZ-derived progenitor cells and track their migratory profile.…”

Section: Excitotoxic Brain Injurymentioning

confidence: 99%

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