PMID- 11003834
OWN - NLM
STAT- MEDLINE
DCOM- 20001120
LR  - 20220215
IS  - 0950-1991 (Print)
IS  - 0950-1991 (Linking)
VI  - 127
IP  - 20
DP  - 2000 Oct
TI  - Positive and negative interactions of GDNF, NTN and ART in developing sensory 
      neuron subpopulations, and their collaboration with neurotrophins.
PG  - 4335-44
AB  - Glial cell line-derived neurotrophic factor (GDNF), neurturin (NTN) and 
      neublastin/artemin (ART) are distant members of the transforming growth factor 
      beta family, and have been shown to elicit neurotrophic effects upon several 
      classes of peripheral and central neurons. Limited information from in vitro and 
      expression studies has also substantiated a role for GDNF family ligands in 
      mammalian somatosensory neuron development. Here, we show that although dorsal 
      root ganglion (DRG) sensory neurons express GDNF family receptors embryonically, 
      they do not survive in response to their ligands. The regulation of survival 
      emerges postnatally for all GDNF family ligands. GDNF and NTN support distinct 
      subpopulations that can be separated with respect to their expression of GDNF 
      family receptors, whereas ART supports neurons in populations that are also 
      responsive to GDNF or NTN. Sensory neurons that coexpress GDNF family receptors 
      are medium sized, whereas small-caliber nociceptive cells preferentially express 
      a single receptor. In contrast to brain-derived neurotrophic factor 
      (BDNF)-dependent neurons, embryonic nerve growth factor (NGF)-dependent 
      nociceptive neurons switch dependency to GDNF, NTN and ART postnatally. Neurons 
      that survive in the presence of neurotrophin 3 (NT3) or neurotrophin 4 (NT4), 
      including proprioceptive afferents, Merkel end organs and D-hair afferents, are 
      also supported by GDNF family ligands neonatally, although at postnatal stages 
      they lose their dependency on GDNF and NTN. At late postnatal stages, ART 
      prevents survival elicited by GDNF and NTN. These data provide new insights on 
      the roles of GDNF family ligands in sensory neuron development.
FAU - Baudet, C
AU  - Baudet C
AD  - Laboratory of Molecular Neurobiology, Medical Biochemistry and Biophysics, 
      Karolinska Institutet, S-171 77 Stockholm, Sweden.
FAU - Mikaels, A
AU  - Mikaels A
FAU - Westphal, H
AU  - Westphal H
FAU - Johansen, J
AU  - Johansen J
FAU - Johansen, T E
AU  - Johansen TE
FAU - Ernfors, P
AU  - Ernfors P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Development
JT  - Development (Cambridge, England)
JID - 8701744
RN  - 0 (Artn protein, mouse)
RN  - 0 (Drosophila Proteins)
RN  - 0 (Gdnf protein, mouse)
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor Receptors)
RN  - 0 (Ligands)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Neurotrophin 3)
RN  - 0 (Neurturin)
RN  - 0 (Nrtn protein, mouse)
RN  - 0 (Proto-Oncogene Proteins)
RN  - EC 2.7.10.1 (Proto-Oncogene Proteins c-ret)
RN  - EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases)
RN  - EC 2.7.10.1 (Ret protein, Drosophila)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - Animals
MH  - Cell Survival
MH  - *Drosophila Proteins
MH  - Ganglia, Spinal/*embryology
MH  - Glial Cell Line-Derived Neurotrophic Factor
MH  - Glial Cell Line-Derived Neurotrophic Factor Receptors
MH  - Ligands
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Mutant Strains
MH  - Nerve Growth Factors/genetics/*metabolism
MH  - Nerve Tissue Proteins/genetics/*metabolism
MH  - Neurons, Afferent/*cytology
MH  - Neurotrophin 3/metabolism
MH  - Neurturin
MH  - Proto-Oncogene Proteins/metabolism
MH  - Proto-Oncogene Proteins c-ret
MH  - Receptor Protein-Tyrosine Kinases/metabolism
EDAT- 2000/09/27 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/09/27 11:00
PHST- 2000/09/27 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/09/27 11:00 [entrez]
AID - 10.1242/dev.127.20.4335 [doi]
PST - ppublish
SO  - Development. 2000 Oct;127(20):4335-44. doi: 10.1242/dev.127.20.4335.