Electrophysiological Differentiation of New Neurons in the Olfactory Bulb

Belluzzi, Ottorino; Benedusi, Mascia; Ackman, James B.; LoTurco, Joseph J.

doi:10.1523/jneurosci.23-32-10411.2003

Cited by 272 publications

(250 citation statements)

References 35 publications

Supporting

Mentioning

235

Contrasting

Unclassified

Order By: Relevance

“…In this study, we show that purified neonatal neuroblasts have large GABAergic currents carried by Cl À with an affinity to GABA comparable with those already reported in postnatal SEZ cells [32,33] and embryonic cortical newborn neurons [34] and that these receptors show benzodiazepine sensitivity. In comparison with neuroblasts, precursors display a lower incidence of GABAergic currents with a much smaller current density, nonetheless modulated by diazepam.…”

Section: Discussionsupporting

confidence: 88%

GABAA Receptor Signaling Induces Osmotic Swelling and Cell Cycle Activation of Neonatal Prominin+ Precursors

et al. 2011

View full text Add to dashboard Cite

Signal-regulated changes in cell size affect cell division and survival and therefore are central to tissue morphogenesis and homeostasis. In this respect, GABA receptors (GABA A Rs) are of particular interest because allowing anions flow across the cell membrane modulates the osmolyte flux and the cell volume. Therefore, we have here investigated the hypothesis that GABA may regulate neural stem cell proliferation by inducing cell size changes. We found that, besides neuroblasts, also neural precursors in the neonatal murine subependymal zone sense GABA via GABA A Rs. However, unlike in neuroblasts, where it induced depolarization-mediated [Ca 21 ] i increase, GABA A Rs activation in precursors caused hyperpolarization. This resulted in osmotic swelling and increased surface expression of epidermal growth factor receptors (EGFRs). Furthermore, activation of GABA A Rs signaling in vitro in the presence of EGF modified the expression of the cell cycle regulators, phosphatase and tensin homolog and cyclin D1, increasing the pool of cycling precursors without modifying cell cycle length. A similar effect was observed on treatment with diazepam. We also demonstrate that GABA and diazepam responsive precursors represent prominin 1 stem cells. Finally, we show that as in in vitro also in in vivo a short administration of diazepam promotes EGFR expression in prominin 1 stem cells causing activation and cell cycle entry. Thus, our data indicate that endogenous GABA is a part of a regulatory mechanism of size and cell cycle entry of neonatal stem cells. Our results also have potential implications for the therapeutic practices that involve exposure to GABA A Rs modulators during neurodevelopment. STEM CELLS 2011;29:307-319 Disclosure of potential conflicts of interest is found at the end of this article.

show abstract

Section: Discussionsupporting

confidence: 88%

GABAA Receptor Signaling Induces Osmotic Swelling and Cell Cycle Activation of Neonatal Prominin+ Precursors

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Type A cells are immature neuroblasts that migrate in chains to the olfactory bulb (OB). 42,43 Evidence suggests that type B cells have an astrocytic nature as they show morphologic characteristics of astrocytes and express astroglial markers, such as glial fibrillary acidic protein (GFAP). The adult SGZ contains two types of stem cells (viz., type I and type II).…”

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

“…During neuronal development, a switch in GABA A responses from depolarization to hyperpolarization (Belluzzi et al, 2003;Carleton et al, 2003;Ge et al, 2006) has been linked to a decrease in [Cl Ϫ ] i (Ben-Ari, 2002). The specific effects of GABA during the early stages of development but not later (after 5 DIV) raised the possibility that this was attributable to this switch.…”

Section: Gaba Depolarizes and Opens L-type Voltage-gated Calcium Chanmentioning

confidence: 99%

“…In the mammalian brain, ongoing neurogenesis maintains neuronal replacement in the olfactory bulb (OB) throughout life (Lois et al, 1996;Belluzzi et al, 2003;Carleton et al, 2003). Newly generated neurons from the subventricular zone (SVZ) migrate through the rostral migratory stream to the olfactory bulb, where they rapidly initiate dendritic growth and establish dendrodendritic contacts with mitral cells and other granule cells (AlvarezBuylla and Garcia-Verdugo, 2002;Bolteus and Bordey, 2004;Lledo and Saghatelyan, 2005).…”

Section: Introductionmentioning

confidence: 99%

GABA Regulates Dendritic Growth by Stabilizing Lamellipodia in Newly Generated Interneurons of the Olfactory Bulb

Gascon¹,

Dayer²,

Sauvain³

et al. 2006

J. Neurosci.

View full text Add to dashboard Cite

The initial formation and growth of dendrites is a critical step leading to the integration of newly generated neurons into postnatal functional networks. However, the cellular mechanisms and extracellular signals regulating this process remain mostly unknown. By directly observing newborn neurons derived from the subventricular zone in culture as well as in olfactory bulb slices, we show that ambient GABA acting through GABA A receptors is essential for the temporal stability of lamellipodial protrusions in dendritic growth cones but did not interfere with filopodia dynamics. Furthermore, we provide direct evidence that ambient GABA is required for the proper initiation and elongation of dendrites by promoting the rapid stabilization of new dendritic segments after their extension. The effects of GABA on the initial formation of dendrites depend on depolarization and Ca 2ϩ influx and are associated with a higher stability of microtubules. Together, our results indicate that ambient GABA is a key regulator of dendritic initiation in postnatally generated olfactory interneurons and offer a mechanism by which this neurotransmitter drives early dendritic growth.

show abstract

Electrophysiological Differentiation of New Neurons in the Olfactory Bulb

Cited by 272 publications

References 35 publications

GABAA Receptor Signaling Induces Osmotic Swelling and Cell Cycle Activation of Neonatal Prominin+ Precursors

GABAA Receptor Signaling Induces Osmotic Swelling and Cell Cycle Activation of Neonatal Prominin+ Precursors

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

GABA Regulates Dendritic Growth by Stabilizing Lamellipodia in Newly Generated Interneurons of the Olfactory Bulb

Contact Info

Product

Resources

About