PMID- 10963876
OWN - NLM
STAT- MEDLINE
DCOM- 20001128
LR  - 20190813
IS  - 0303-7207 (Print)
IS  - 0303-7207 (Linking)
VI  - 163
IP  - 1-2
DP  - 2000 May 25
TI  - Neurotrophic and cell-cell dependent control of early follicular development.
PG  - 67-71
AB  - Neurotrophins (NTs) and their receptors play an essential role in the 
      differentiation and survival of defined neuronal populations of the central and 
      peripheral nervous systems. Their actions, however, do not appear to be limited 
      to the nervous system, as both NTs and their receptors have been found in non 
      neuronal cells, including cells of the endocrine system. At least four of the 
      five known neurotrophins, including nerve growth factor (NGF), brain-derived 
      neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4), and 
      their receptors (p75 NTR, trkA, trkB and trkC) are present in the developing 
      ovary. Using mice carrying null mutations of the genes encoding neurotrophins 
      (NGF, NT-4, BDNF) or the receptor that mediates the actions of NT-4 and BDNF 
      (trkB), we have obtained initial results consistent with the notion that 
      neurotrophins are required for the growth of primordial follicles. NGF-deficient 
      mice show a decreased formation of both primary and secondary preantral 
      follicles. Null mutation of the NT-4 gene failed to affect either 
      folliculogenesis or follicular development. However, formation of primary and 
      secondary follicles was compromised in mice carrying a null mutation of both the 
      NT-4 and BDNF genes, suggesting compensation of function by BDNF in NT-4 
      knockouts. Support for this concept is provided by the similar deficiency in 
      follicular growth observed in animals carrying a null mutation of the gene 
      encoding trkB, the receptors mediating NT-4 and BDNF actions. Initial 
      experiments, using differential display, to isolate genes that may be involved in 
      the process of folliculogenesis and/or early follicular development, resulted in 
      the isolation of a recently identified cell adhesion molecule and a novel 
      transcription factor originally shown to induce cell transformation. It thus 
      appears that formation and development of mammalian follicles requires the 
      concerted action of genes originally thought to be only involved in cell 
      differentiation/survival of neuronal cells, and genes that may control the 
      growth, differentiation, and cell-cell interactions of somatic and germ cells in 
      the ovary.
FAU - Ojeda, S R
AU  - Ojeda SR
AD  - Divisions of Neuroscience, Oregon Regional Primate Research Center/Oregon Health 
      Sciences University, 505 N.W. 185th Avenue, Beaverton, OR 97006, USA. 
      ojedas@ohsu.edu
FAU - Romero, C
AU  - Romero C
FAU - Tapia, V
AU  - Tapia V
FAU - Dissen, G A
AU  - Dissen GA
LA  - eng
GR  - HD24870/HD/NICHD NIH HHS/United States
GR  - RR00163/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - Ireland
TA  - Mol Cell Endocrinol
JT  - Molecular and cellular endocrinology
JID - 7500844
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Neurotrophin 3)
RN  - 0 (Receptor, Nerve Growth Factor)
RN  - 0 (Receptors, Nerve Growth Factor)
RN  - 9061-61-4 (Nerve Growth Factor)
RN  - EC 2.7.10.1 (Receptor, trkA)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - P658DCA9XD (neurotrophin 4)
SB  - IM
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/physiology
MH  - Female
MH  - Nerve Growth Factor/physiology
MH  - Nerve Growth Factors/genetics/*physiology
MH  - Neurotrophin 3/physiology
MH  - Ovarian Follicle/innervation/*physiology
MH  - Receptor, Nerve Growth Factor/physiology
MH  - Receptor, trkA/physiology
MH  - Receptor, trkB/physiology
MH  - Receptors, Nerve Growth Factor/*physiology
MH  - *Signal Transduction
RF  - 45
EDAT- 2000/08/30 11:00
MHDA- 2001/02/28 10:01
CRDT- 2000/08/30 11:00
PHST- 2000/08/30 11:00 [pubmed]
PHST- 2001/02/28 10:01 [medline]
PHST- 2000/08/30 11:00 [entrez]
AID - S0303-7207(99)00242-7 [pii]
AID - 10.1016/s0303-7207(99)00242-7 [doi]
PST - ppublish
SO  - Mol Cell Endocrinol. 2000 May 25;163(1-2):67-71. doi: 
      10.1016/s0303-7207(99)00242-7.