PMID- 16097493
OWN - NLM
STAT- MEDLINE
DCOM- 20050916
LR  - 20220129
IS  - 0003-9829 (Print)
IS  - 0003-9829 (Linking)
VI  - 143
IP  - 3-4
DP  - 2005 Sep
TI  - Factors involved in the migration of neuroendocrine hypothalamic neurons.
PG  - 171-8
AB  - Neuroendocrine control of physiological functions needs a complex developmental 
      organisation of the hypothalamic parvicellular neurons, which synthesise and 
      release hypophysiotropic hormones. Among the hypothalamic neuroendocrine cells, 
      Gonadotropin-releasing hormone (GnRH) neurons represent a unique class; they are 
      generated in the olfactory placode and, during embryonic life, migrate to the 
      septo/hypothalamic region along terminal and vomeronasal nerves. At this level 
      GnRH neurons undergo terminal differentiation and start to release GnRH to 
      modulate the secretion of pituitary gonadotropins. All these steps are under the 
      strict control of several developmental cues and their defect might represent a 
      cause of clinical disorders. A number of factors have been proposed to be 
      involved in the migration of GnRH neurons, but their role is still unclear. By 
      using gene knockout techniques it has been found that mice carrying a targeted 
      deletion of Ebf2 gene, a component of Olf/Ebf bHLH transcription factors, show a 
      defective migration of GnRH neurons, providing the first evidence of a mouse 
      model of such defect. Since the investigation of GnRH neurons is hindered by 
      their peculiar anatomical distribution, other studies has been forwarded by the 
      availability of immortalized GnRH-expressing neurons (GN11 cells) that retain a 
      strong chemomigratory response "in vitro". Among the factors analysed, we found 
      that hepatocyte growth factor/scatter factor (HGF/SF) and vascular endothelial 
      growth factor (VEGF) induce specific chemotaxis of GN 11 neurons, suggesting that 
      migratory signals can arise from nasal mesenchyme and from the concomitant 
      vasculogenesis. Finally, anosmin-1 (the product of the gene responsible of the 
      X-linked form of Kallmann's disease) was found to induce a significant 
      chemotactic response of GN11 cells, confirming a permissive/instructive role of 
      KAL1 gene product in the migratory behaviour of GnRH neurons. In conclusion, the 
      migration of the GnRH neurons appears to be a complex process, which involves the 
      interplay of multiple molecular cues. These studies may provide new insights on 
      the etiopathogenesis of the large proportion of reproductive dysfunctions that 
      affect humans and could provide novel insights on common biochemical events 
      controlling neuronal development and migration.
FAU - Maggi, R
AU  - Maggi R
AD  - Laboratory of Developmental Neuroendocrinology, Department of Endocrinology, 
      Centre of Excellence on Neurodegenerative Diseases, University of Milano, Via G. 
      Balzaretti 9, 20133 Milano, Italy. roberto.maggi@unimi.it
FAU - Cariboni, A
AU  - Cariboni A
FAU - Zaninetti, R
AU  - Zaninetti R
FAU - Samara, A
AU  - Samara A
FAU - Stossi, F
AU  - Stossi F
FAU - Pimpinelli, F
AU  - Pimpinelli F
FAU - Giacobini, P
AU  - Giacobini P
FAU - Consalez, G G
AU  - Consalez GG
FAU - Rugarli, E
AU  - Rugarli E
FAU - Piva, F
AU  - Piva F
LA  - eng
GR  - TGM03P08/TI_/Telethon/Italy
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
PL  - Italy
TA  - Arch Ital Biol
JT  - Archives italiennes de biologie
JID - 0372441
RN  - 0 (Nerve Growth Factors)
RN  - 33515-09-2 (Gonadotropin-Releasing Hormone)
SB  - IM
MH  - Animals
MH  - Cell Movement/*physiology
MH  - Gene Expression Regulation, Developmental/genetics
MH  - Gonadotropin-Releasing Hormone/*metabolism
MH  - Humans
MH  - Hypothalamo-Hypophyseal System/embryology/metabolism
MH  - Hypothalamus/cytology/*embryology/metabolism
MH  - Nerve Growth Factors/genetics/metabolism
MH  - Neurons/cytology/*metabolism
MH  - Neurosecretory Systems/cytology/*embryology/metabolism
MH  - Signal Transduction/physiology
RF  - 19
EDAT- 2005/08/16 09:00
MHDA- 2005/09/17 09:00
CRDT- 2005/08/16 09:00
PHST- 2005/08/16 09:00 [pubmed]
PHST- 2005/09/17 09:00 [medline]
PHST- 2005/08/16 09:00 [entrez]
PST - ppublish
SO  - Arch Ital Biol. 2005 Sep;143(3-4):171-8.