Impairment of neural precursor proliferation increases survival of cell progeny in the adult rat dentate gyrus

Ciaroni, Sandra; Cecchini, Tiziana; Ferri, Paola; Ambrogini, Patrizia; Cuppini, Riccardo; Riccio, Massimo; Lombardelli, G.; Papa, Stefano; Grande, Paolo Del

doi:10.1016/s0047-6374(02)00070-2

Cited by 22 publications

(15 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For instance, experimental increases in the PCD of adult DG cells induced by adrenalectomy and excitotoxic or mechanical lesions increases neurogenesis (Cameron and Gould, 1994;Liu et al, 1998;Yoshimura et al, 2001), and experimentally induced apoptosis also selectively increases the number of adult-generated neurons (Magavi et al, 2000). Conversely, experimental inhibition of adult neural stem cell proliferation by injection of a mitotic inhibitor increases the survival rate of the progeny (Ciaroni et al, 2002). In contrast, our observations do not support such a relationship.…”

Section: Proliferation Is Not Directly Altered By the Elimination Of contrasting

confidence: 84%

Programmed Cell Death of Adult-Generated Hippocampal Neurons Is Mediated by the Proapoptotic Gene Bax

Sun¹,

Winseck²,

Vinsant³

et al. 2004

J. Neurosci.

178

197

View full text Add to dashboard Cite

In the dentate gyrus (DG) of the adult mouse hippocampus, a substantial number of new cells are generated daily, but only a subset of these survive and differentiate into mature neurons, whereas the majority undergo programmed cell death (PCD). However, neither the intracellular machinery required for adult stem cell-derived neuronal death nor the biological implications of the significant loss of these newly generated cells have been examined. Several markers for apoptosis failed to reveal cell death in Bax-deficient mice, and this, together with a progressive increase in neuron number in the DG of the Bax knock-out, indicates that Bax is critical for the PCD of adult-generated hippocampal neurons. Whereas the proliferation of neural progenitor cells was not altered in the Bax-knock-out, there was an accumulation of doublecortin, calretinin ϩ , and neuronal-specific nuclear protein ϩ postmitotic neurons, suggesting that Baxmediated PCD of adult-generated neurons takes place during an early phase of differentiation. The absence of PCD in the adult also influenced the migration and maturation of adult-generated DG neurons. These results suggest that PCD in the adult brain plays a significant role in the regulation of multiple aspects of adult neurogenesis.

show abstract

Section: Proliferation Is Not Directly Altered By the Elimination Of contrasting

confidence: 84%

Programmed Cell Death of Adult-Generated Hippocampal Neurons Is Mediated by the Proapoptotic Gene Bax

Sun¹,

Winseck²,

Vinsant³

et al. 2004

J. Neurosci.

178

197

View full text Add to dashboard Cite

show abstract

“…The fact that when undifferentiated NSCs were grafted into 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine damaged brains, the majority of new dopaminergic neurons were "rescued" host cells (Ourednik et al, 2002) opens the possibility that undifferentiated progenitors might spontaneously express neuroprotective signals, and that NSCs might have an inherent capacity to alter the host environment, reactivating or preserving dysfunctional endogenous neurons. Previous studies (Ciaroni et al, 2002) describe a correlation between proliferation and cell survival. If proliferation is inhibited, the rate of survival increases.…”

Section: Discussionmentioning

confidence: 97%

Neurogenic Effect of -Amyloid Peptide in the Development of Neural Stem Cells

López‐Toledano

Shelanski²

2004

Journal of Neuroscience

220

160

View full text Add to dashboard Cite

The adult mammalian brain contains neural stem cells (NSCs) with self-renewal and multilineage potential in the hippocampus and subventricular zone. However, neurogenesis from these areas does not compensate for neuronal loss in age-related neurodegenerative disorders such as Alzheimer's disease (AD). To test whether an impairment of neurogenesis could contribute to the pathogenesis of AD, we examined the effects of amyloid-␤ peptide (A␤) on the survival and neuronal differentiation of cultured NSCs from striatum and hippocampus. We show that A␤ peptide does not impair the neurogenic rate in NSC progeny, but that it increases the total number of neurons in vitro in a dose-dependent manner. The neurogenic effect of A␤ peptide is not dependent on soluble factors released from the NSC progeny. Neurogenesis is induced by A␤42 and not A␤40 or A␤ 25-35, and the activity appears to be a property of A␤ oligomers and not fibrils.These results suggest that A␤ may have positive as well as deleterious actions, and that a knowledge of the mechanisms involved in the former could be valuable in exploiting the regenerative and plastic potential of the brain in preventing and treating Alzheimer's disease.

show abstract

“…The outlines of the granule cell nuclei were drawn at the final magnification of 788× and their diameter, used in Abercrombie’s formula [27], was calculated by means of Optilab software. Mean granule cell number/mm 3 was estimated by counting the number of plotted neurons in sample fields randomly chosen within dentate gyrus blades at the final magnification of 500×, as previously described [28]. For this purpose, 1 in every 40 sections, i.e.…”

Section: Methodsmentioning

confidence: 99%

Thyroid Hormones Affect Neurogenesis in the Dentate Gyrus of Adult Rat

et al. 2005

Self Cite

View full text Add to dashboard Cite

Thyroid hormones play a crucial role in new neuron production and maturation during brain development. However, the knowledge about the involvement of these hormones on adult neurogenesis is still incomplete. Hippocampus is an anatomical region where neurogenesis occurs throughout adulthood and where high levels of thyroid hormone receptors have been found. In this work the possible involvement of thyroid hormones in the regulation of adult neurogenesis in the granule cell layer of rat hippocampus dentate gyrus was investigated using an experimental model of adult-onset pharmacologically-induced hypothyroidism. Neurogenesis was assessed by means of the thymidine analogue 5-bromo-2′-deoxyuridine 24 h and 30 days after its last administration in order to study neural precursor proliferation and newborn cell survival, respectively. Mitotic activity of the neural precursors was not affected by thyroid hormone deficiency; on the contrary, newborn cell survival dramatically decreased under these conditions when compared with controls, leading to a lower number of immature neurons being added to the granule cell layer. Moreover, in conditions of hypothyroidism, new neurons exhibit a delay in neuronal differentiation showing a prolonged expression of the neuritogenesis-associated immature neuron marker TUC-4 and a very immature morphology. Finally, the total number and size of granule cells, and granule cell layer volume decreased in hypothyroid rats. These results suggest that thyroid hormones play a role in regulating new neuron production during adult life in dentate gyrus of rat hippocampus.

show abstract

Impairment of neural precursor proliferation increases survival of cell progeny in the adult rat dentate gyrus

Cited by 22 publications

References 46 publications

Programmed Cell Death of Adult-Generated Hippocampal Neurons Is Mediated by the Proapoptotic Gene Bax

Programmed Cell Death of Adult-Generated Hippocampal Neurons Is Mediated by the Proapoptotic Gene Bax

Neurogenic Effect of -Amyloid Peptide in the Development of Neural Stem Cells

Thyroid Hormones Affect Neurogenesis in the Dentate Gyrus of Adult Rat

Contact Info

Product

Resources

About