PMID- 10331972
OWN - NLM
STAT- MEDLINE
DCOM- 19990722
LR  - 20220215
IS  - 0950-1991 (Print)
IS  - 0950-1991 (Linking)
VI  - 126
IP  - 12
DP  - 1999 Jun
TI  - A rapid and dynamic regulation of GDNF-family ligands and receptors correlate
      with the developmental dependency of cutaneous sensory innervation.
PG  - 2597-610
AB  - Glial cell line-derived neurotrophic factor (GDNF) and neurturin (NTN) are
      members of the transforming growth factor-beta family and have been shown to
      elicit neurotrophic effects upon several classes of neurons including
      dopaminergic neurons, motoneurons, parasympathetic, sympathetic as well as
      primary sensory neurons. However, there is little information available on their 
      roles in cutaneous innervation. Herein, we have studied the regulation of gdnf,
      ntn and the GDNF family receptors and examined their role in the development of
      facial cutaneous innervation in GDNF mutant mice. A dynamic spatial and temporal 
      regulation of gdnf, ntn and their ligand binding receptors within the
      follicle-sinus complex correlate with development of distinct subclasses of
      sensory nerve endings. Furthermore, development of NGF-dependent myelinated
      mechanoreceptors, i.e. reticular and transverse lanceolate endings also require
      GDNF during ending formation and maintenance. In addition, ligand and receptor
      association seems to be intricately linked to a local Schwann cell-axon
      interaction essential for sensory terminal formation. Our results suggests that
      functionally specified nerve endings depend on different GDNF family members and 
      that in contrast to neurotrophins, this family of neurotrophic factors may be
      acting at local sites of terminal Schwann cell-axon growth cone interactions and 
      that they collaborate with neurotrophins by supporting the same populations of
      neurons but at different times in development.
FAU - Fundin, B T
AU  - Fundin BT
AD  - Laboratory of Molecular Neurobiology, MBB, Karolinska Institute, S171 77
      Stockholm, Sweden. Bengt@cajal.mbb.ki.se
FAU - Mikaels, A
AU  - Mikaels A
FAU - Westphal, H
AU  - Westphal H
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 (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 (Membrane Glycoproteins)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (Neurturin)
RN  - 0 (Nrtn protein, mouse)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Receptors, Nerve Growth Factor)
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)
SB  - IM
MH  - Animals
MH  - Axons/metabolism
MH  - *Drosophila Proteins
MH  - Face/innervation
MH  - Gene Expression Regulation, Developmental
MH  - Glial Cell Line-Derived Neurotrophic Factor
MH  - Glial Cell Line-Derived Neurotrophic Factor Receptors
MH  - Hair Follicle/innervation
MH  - *Membrane Glycoproteins
MH  - Mice
MH  - Mice, Mutant Strains
MH  - Myelin Sheath/physiology
MH  - Nerve Growth Factors/genetics/metabolism
MH  - Nerve Tissue Proteins/genetics/metabolism
MH  - Neurites/metabolism
MH  - Neurons, Afferent/*physiology
MH  - Neurturin
MH  - Proto-Oncogene Proteins/*genetics/metabolism
MH  - Proto-Oncogene Proteins c-ret
MH  - Receptor Protein-Tyrosine Kinases/*genetics/metabolism
MH  - Receptors, Cell Surface/genetics/metabolism
MH  - *Receptors, Nerve Growth Factor
MH  - Schwann Cells/metabolism
MH  - Skin/*innervation
MH  - Trigeminal Ganglion/metabolism
MH  - Vibrissae/innervation
EDAT- 1999/05/20 00:00
MHDA- 1999/05/20 00:01
CRDT- 1999/05/20 00:00
PHST- 1999/05/20 00:00 [pubmed]
PHST- 1999/05/20 00:01 [medline]
PHST- 1999/05/20 00:00 [entrez]
AID - 10.1242/dev.126.12.2597 [doi]
PST - ppublish
SO  - Development. 1999 Jun;126(12):2597-610. doi: 10.1242/dev.126.12.2597.