Reelin Regulates Neuronal Progenitor Migration in Intact and Epileptic Hippocampus

Gong, Chao; Wang, Tsu Wei; Huang, Holly S.; Parent, Jack M.

doi:10.1523/jneurosci.3111-06.2007

Cited by 208 publications

(180 citation statements)

References 66 publications

Supporting

Mentioning

167

Contrasting

Order By: Relevance

“…Given that Reelin deficiency also leads to abnormal neuronal migration and lamination (Drakew et al, 2002;Zhao et al, 2004;Gong et al, 2007), our results suggest that Reelin levels, both below and above a certain threshold, impair neuronal migration. However, it is also possible that the ectopic expression of Reelin in the GL of adult Tg1/Tg2 mice contributes to the altered migration observed in the DG.…”

Section: Reelin Control Of Adult Neurogenesis and Migrationmentioning

confidence: 74%

Reelin Regulates Postnatal Neurogenesis and Enhances Spine Hypertrophy and Long-Term Potentiation

Pujadas¹,

Gruart²,

Bosch³

et al. 2010

J. Neurosci.

194

207

View full text Add to dashboard Cite

Reelin, an extracellular protein essential for neural migration and lamination, is also expressed in the adult brain. To unravel the function of this protein in the adult forebrain, we generated transgenic mice that overexpress Reelin under the control of the CaMKII␣ promoter. Overexpression of Reelin increased adult neurogenesis and impaired the migration and positioning of adult-generated neurons. In the hippocampus, the overexpression of Reelin resulted in an increase in synaptic contacts and hypertrophy of dendritic spines. Induction of long-term potentiation (LTP) in alert-behaving mice showed that Reelin overexpression evokes a dramatic increase in LTP responses. Hippocampal field EPSP during a classical conditioning paradigm was also increased in these mice. Our results indicate that Reelin levels in the adult brain regulate neurogenesis and migration, as well as the structural and functional properties of synapses. These observations suggest that Reelin controls developmental processes that remain active in the adult brain.

show abstract

Section: Reelin Control Of Adult Neurogenesis and Migrationmentioning

confidence: 74%

Reelin Regulates Postnatal Neurogenesis and Enhances Spine Hypertrophy and Long-Term Potentiation

Pujadas¹,

Gruart²,

Bosch³

et al. 2010

J. Neurosci.

194

207

View full text Add to dashboard Cite

show abstract

“…Cajal Retzius cells express Reelin that functions as a guiding signal for radially migrating cells and thereby maintains a normal cell integration in the DG (Gong et al, 2007). Reelin was clearly expressed in the external blade of wild-type DGs, while in mutants its staining reflected the truncation of the external blade (Fig.…”

Section: Impaired Dg In Newborn and Adult D6-dkk1 Micementioning

confidence: 97%

Effect of canonical Wnt inhibition in the neurogenic cortex, hippocampus, and premigratory dentate gyrus progenitor pool

Solberg

Machoň

Krauß

2008

Developmental Dynamics

View full text Add to dashboard Cite

Canonical Wnt signaling is crucial for the correct development of both cortical and hippocampal structures in the dorsal telencephalon. In this study, we examined the role of the canonical Wnt signaling in the dorsal telencephalon of mouse embryos at defined time periods by inhibition of the pathway with ectopic expression of Dkk1. Transgenic mice with the D6-driven Dkk1 gene exhibited reduced canonical Wnt signaling in the cortex and hippocampus. As a result, all hippocampal fields were reduced in size. Neurogenesis in the dentate gyrus was severely reduced both in the premigratory and migratory progenitor pool. The lower number of progenitors in the dentate gyrus was not rescued after migration to the subgranular zone and thus the dentate gyrus lacked the entire internal blade and a part of the external blade from postnatal to adult stages.

show abstract

“…The examples include considerable increases in the dentate neurogenesis observed in the young brain after ischemia, stroke or hypoxic injury (Liu et al ., 1998;Jin et al ., 2001Jin et al ., , 2004 and acute seizures or status epilepticus induced through excitotoxins or cholinomimetic chemicals (Bengzon et al ., 1997;Parent et al ., 1997Parent et al ., , 2006Gray & Sundstrom, 1998;Hattiangady et al ., 2004;Gong et al ., 2007). Although the precise benefits or adverse effects of increased neurogenesis after brain injury are still being studied (Parent, 2003;Jessberger et al ., 2007;, it is generally believed that this plasticity is useful for reducing impairments in cognitive functions after brain injury (Kleindienst et al ., 2005;Sun et al ., 2007).…”

Section: Introductionmentioning

confidence: 99%

Plasticity of hippocampal stem/progenitor cells to enhance neurogenesis in response to kainate‐induced injury is lost by middle age

2007

View full text Add to dashboard Cite

SummaryA remarkable up-regulation of neurogenesis through increased proliferation of neural stem/progenitor cells (NSCs) is a well-known plasticity displayed by the young dentate gyrus (DG) following brain injury. To ascertain whether this plasticity is preserved during aging, we quantified DG neurogenesis in the young adult, middleaged and aged F344 rats after kainic acid induced hippocampal injury. Measurement of new cells that are added to the dentate granule cell layer (GCL) between post-injury days 4 and 15 using 5′ ′ ′ ′ -bromodeoxyuridine labeling revealed an increased addition of new cells in the young DG but not in the middle-aged and aged DG. Quantification of newly born neurons using doublecortin immunostaining also demonstrated a similar trend. Furthermore, the extent of ectopic migration of new neurons into the dentate hilus was dramatically increased in the young DG but was unaltered in the middle-aged and aged DG. However, there was no change in neuronal fate-choice decision of newly born cells following injury in all age groups. Similarly, comparable fractions of new cells that are added to the GCL after injury exhibited 5-month survival and expressed the mature neuronal marker NeuN, regardless of age or injury at the time of their birth. Thus, hippocampal injury does not adequately stimulate NSCs in the middle-aged and aged DG, resulting in no changes in neurogenesis after injury. Interestingly, rates of both neuronal fate-choice decision and long-term survival of newly born cells remain stable with injury in all age groups. These results underscore that the ability of the DG to increase neurogenesis after injury is lost as early as middle age.

show abstract

Reelin Regulates Neuronal Progenitor Migration in Intact and Epileptic Hippocampus

Cited by 208 publications

References 66 publications

Reelin Regulates Postnatal Neurogenesis and Enhances Spine Hypertrophy and Long-Term Potentiation

Reelin Regulates Postnatal Neurogenesis and Enhances Spine Hypertrophy and Long-Term Potentiation

Effect of canonical Wnt inhibition in the neurogenic cortex, hippocampus, and premigratory dentate gyrus progenitor pool

Plasticity of hippocampal stem/progenitor cells to enhance neurogenesis in response to kainate‐induced injury is lost by middle age

Contact Info

Product

Resources

About