Highly polysialylated neural cell adhesion molecule (NCAM-H) is expressed by newly generated granule cells in the dentate gyrus of the adult rat

Seki, Tatsunori; Arai, Yasumasa

doi:10.1523/jneurosci.13-06-02351.1993

Cited by 442 publications

(304 citation statements)

References 35 publications

Supporting

Mentioning

280

Contrasting

Unclassified

Order By: Relevance

“…44,45 Immature type II progenitors cells divide and will later show properties of neurons, e.g., express doublecortin (DCX), poly-sialylated neural adhesion molecule (PSA-NCAM), or neuronal nuclei (NeuN). 7,45,47 Until recently, NSCs had only been observed in the SVZ and SGZ of the healthy mammalian brain. However, an intriguing study identified neural progenitor cells in the neocortical layer 1 of adult rats subjected to mild ischemia.…”

Section: The Developing Mammalian Brainmentioning

confidence: 99%

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

Donega

Velthoven

Nijboer

et al. 2013

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Neurogenesis continues throughout adulthood. The neurogenic capacity of the brain increases after injury by, e.g., hypoxiaischemia. However, it is well known that in many cases brain damage does not resolve spontaneously, indicating that the endogenous regenerative capacity of the brain is insufficient. Neonatal encephalopathy leads to high mortality rates and long-term neurologic deficits in babies worldwide. Therefore, there is an urgent need to develop more efficient therapeutic strategies. The latest findings indicate that stem cells represent a novel therapeutic possibility to improve outcome in models of neonatal encephalopathy. Transplanted stem cells secrete factors that stimulate and maintain neurogenesis, thereby increasing cell proliferation, neuronal differentiation, and functional integration. Understanding the molecular and cellular mechanisms underlying neurogenesis after an insult is crucial for developing tools to enhance the neurogenic capacity of the brain. The aim of this review is to discuss the endogenous capacity of the neonatal brain to regenerate after a cerebral ischemic insult. We present an overview of the molecular and cellular mechanisms underlying endogenous regenerative processes during development as well as after a cerebral ischemic insult. Furthermore, we will consider the potential to use stem cell transplantation as a means to boost endogenous neurogenesis and restore brain function.

show abstract

Section: The Developing Mammalian Brainmentioning

confidence: 99%

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

Donega

Velthoven

Nijboer

et al. 2013

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…The de-adhesive properties of PSA-NCAMs have been suggested to counteract the stressinduced excess glutamatergic input (Hoffman et al, 1997;Rutishauser, 1998;Sandi, 2004) and/or the reduction in BDNF that follows chronic stress protocols (Smith et al, 1995). As polysialylation of NCAM is critical for neurogenesis (Seki and Arai, 1993;Franceschini et al, 2001) and for synaptic plasticity (Muller et al, 1996), increased PSA-NCAM expression levels were suggested to represent a compensatory response to the deleterious structural effects of stress (Sandi et al, 2001). …”

Section: Exposure To Stress During Juvenility Alters Emotional Responmentioning

confidence: 99%

Exposure to Stressors during Juvenility Disrupts Development-Related Alterations in the PSA-NCAM to NCAM Expression Ratio: Potential Relevance for Mood and Anxiety Disorders

Tsoory

Guterman

Richter‐Levin

2007

Neuropsychopharmacol

View full text Add to dashboard Cite

Childhood trauma is associated with higher rates of both mood and anxiety disorders in adulthood. The exposure of rats to stressors during juvenility has comparable effects, and was suggested as a model of induced predisposition for these disorders. The neural cell adhesion molecule (NCAM) and its polysialylated form PSA-NCAM are critically involved in neural development, activity-dependent synaptic plasticity, and learning processes. We examined the effects of exposure to stressors during juvenility on coping with stressors in adulthood and on NCAM and PSA-NCAM expression within the rat limbic system both soon after the exposure and in adulthood. Exposure to stressors during juvenility reduced novel-setting exploration and impaired two-way shuttle avoidance learning in adulthood. Among naive rats, a development-related decrease of about 50% was evident in the PSA-NCAM to NCAM expression ratio in the basolateral amygdala, in the CA1 and dentate gyrus regions of the hippocampus, and in the entorhinal cortex. In juvenile-stressed rats, we found no such decrease, but rather an increase in the polysialylation of NCAM (B50%), evident soon after the exposure to juvenile stress and also in adulthood. Our results suggest that exposure to stressors during juvenility alters the maturation of the limbic system, and potentially underlies the predisposition to exhibit stress-related symptoms in adulthood.

show abstract

“…In the adult mammalian hippocampus PSA-NCAM expression is mainly located in a subpopulation of granule cells located in the innermost region of the granular layer of the dentate gyrus (Seki andArai 1991). Many of these cells are recently generated neurones (Seki and Arai 1993), which could be migrating to upper rows of the granule cell layer or extending their projections.…”

Section: Migration and Maturation Of Newly Generated Neuronesmentioning

confidence: 99%

The lizard cerebral cortex as a model to study neuronal regeneration

López‐García

Molowny

Nácher

et al. 2002

An. Acad. Bras. Ciênc.

View full text Add to dashboard Cite

The medial cerebral cortex of lizards, an area homologous to the hippocampal fascia dentata, shows delayed postnatal neurogenesis, i.e., cells in the medial cortex ependyma proliferate and give rise to immature neurons, which migrate to the cell layer. There, recruited neurons differentiate and give rise to zinc containing axons directed to the rest of cortical areas, thus resulting in a continuous growth of the medial cortex and its zincenriched axonal projection. This happens along the lizard life span, even in adult lizards, thus allowing one of their most important characteristics: neuronal regeneration. Experiments in our laboratory have shown that chemical lesion of the medial cortex (affecting up to 95% of its neurons) results in a cascade of events: first, massive neuronal death and axonal-dendritic retraction and, secondly, triggered ependymal-neuroblast proliferation and subsequent neo-histogenesis and regeneration of an almost new medial cortex, indistinguishable from a normal undamaged one. This is the only case to our knowledge of the regeneration of an amniote central nervous centre by new neuron production and neo-histogenesis. Thus the lizard cerebral cortex is a good model to study neuronal regeneration and the complex factors that regulate its neurogenetic, migratory and neo-synaptogenetic events.

show abstract

Highly polysialylated neural cell adhesion molecule (NCAM-H) is expressed by newly generated granule cells in the dentate gyrus of the adult rat

Cited by 442 publications

References 35 publications

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

The Endogenous Regenerative Capacity of the Damaged Newborn Brain: Boosting Neurogenesis with Mesenchymal Stem Cell Treatment

Exposure to Stressors during Juvenility Disrupts Development-Related Alterations in the PSA-NCAM to NCAM Expression Ratio: Potential Relevance for Mood and Anxiety Disorders

The lizard cerebral cortex as a model to study neuronal regeneration

Contact Info

Product

Resources

About