PMID- 17494700
OWN - NLM
STAT- MEDLINE
DCOM- 20070622
LR  - 20200225
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Print)
IS  - 0270-6474 (Linking)
VI  - 27
IP  - 19
DP  - 2007 May 9
TI  - p75 neurotrophin receptor expression defines a population of BDNF-responsive 
      neurogenic precursor cells.
PG  - 5146-55
AB  - Although our understanding of adult neurogenesis has increased dramatically over 
      the last decade, confusion still exists regarding both the identity of the stem 
      cell responsible for neuron production and the mechanisms that regulate its 
      activity. Here we show, using flow cytometry, that a small population of cells 
      (0.3%) within the stem cell niche of the rat subventricular zone (SVZ) expresses 
      the p75 neurotrophin receptor (p75(NTR)) and that these cells are responsible for 
      neuron production in both newborn and adult animals. In the adult, the 
      p75(NTR)-positive population contains all of the neurosphere-producing precursor 
      cells, whereas in the newborn many of the precursor cells are p75(NTR) negative. 
      However, at both ages, only the neurospheres derived from p75(NTR)-positive cells 
      are neurogenic. We also show that neuron production from p75(NTR)-positive but 
      not p75(NTR)-negative precursors is greatly enhanced after treatment with 
      brain-derived neurotrophic factor (BDNF) or nerve growth factor. This effect 
      appears to be mediated specifically by p75(NTR), because precursor cells from 
      p75(NTR)-deficient mice show a 70% reduction in their neurogenic potential in 
      vitro and fail to respond to BDNF treatment. Furthermore, adult 
      p75(NTR)-deficient mice have significantly reduced numbers of PSA-NCAM 
      (polysialylated neural cell adhesion molecule)-positive SVZ neuroblasts in vivo 
      and a lower olfactory bulb weight. Thus, p75(NTR) defines a discrete population 
      of highly proliferative SVZ precursor cells that are able to respond to 
      neurotrophin activation by increasing neuroblast generation, making this pathway 
      the most likely mechanism for the increased neurogenesis that accompanies raised 
      BDNF levels in a variety of disease and behavioral situations.
FAU - Young, Kaylene M
AU  - Young KM
AD  - Queensland Brain Institute, The University of Queensland, Brisbane QLD 4072, 
      Australia.
FAU - Merson, Tobias D
AU  - Merson TD
FAU - Sotthibundhu, Areechun
AU  - Sotthibundhu A
FAU - Coulson, Elizabeth J
AU  - Coulson EJ
FAU - Bartlett, Perry F
AU  - Bartlett PF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (Biomarkers)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Neural Cell Adhesion Molecule L1)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - 0 (Sialic Acids)
RN  - 0 (polysialyl neural cell adhesion molecule)
SB  - IM
MH  - Aging/physiology
MH  - Animals
MH  - Animals, Newborn
MH  - Biomarkers/metabolism
MH  - Brain/cytology/*growth & development/*metabolism
MH  - Brain-Derived Neurotrophic Factor/*metabolism/pharmacology
MH  - Cell Differentiation/genetics
MH  - Cell Lineage/physiology
MH  - Cell Movement/physiology
MH  - Cell Proliferation/drug effects
MH  - Cells, Cultured
MH  - Gene Expression Regulation, Developmental/genetics
MH  - Mice
MH  - Mice, Knockout
MH  - Neural Cell Adhesion Molecule L1/metabolism
MH  - Neurons/cytology/*metabolism
MH  - Olfactory Bulb/cytology/growth & development/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptor, Nerve Growth Factor/genetics/*metabolism
MH  - Sialic Acids/metabolism
MH  - Spheroids, Cellular
MH  - Stem Cells/cytology/drug effects/*metabolism
MH  - Telencephalon/cytology/embryology/metabolism
PMC - PMC6672366
EDAT- 2007/05/15 09:00
MHDA- 2007/06/23 09:00
PMCR- 2007/11/09
CRDT- 2007/05/15 09:00
PHST- 2007/05/15 09:00 [pubmed]
PHST- 2007/06/23 09:00 [medline]
PHST- 2007/05/15 09:00 [entrez]
PHST- 2007/11/09 00:00 [pmc-release]
AID - 27/19/5146 [pii]
AID - 3217387 [pii]
AID - 10.1523/JNEUROSCI.0654-07.2007 [doi]
PST - ppublish
SO  - J Neurosci. 2007 May 9;27(19):5146-55. doi: 10.1523/JNEUROSCI.0654-07.2007.