PMID- 10453054
OWN - NLM
STAT- MEDLINE
DCOM- 19991004
LR  - 20191103
IS  - 0022-3034 (Print)
IS  - 0022-3034 (Linking)
VI  - 40
IP  - 4
DP  - 1999 Sep 15
TI  - Glial-neuronal interactions in the neuroendocrine control of mammalian puberty: 
      facilitatory effects of gonadal steroids.
PG  - 528-40
AB  - It is now clear that astroglial cells actively contribute to both the generation 
      and flow of information within the central nervous system. In the hypothalamus, 
      astrocytes regulate the secretory activity of neuroendocrine neurons. A small 
      subset of these neurons secrete luteinizing hormone-releasing hormone (LHRH), a 
      neuropeptide essential for sexual development and adult reproductive function. 
      Astrocytes stimulate LHRH secretion via cell-cell signaling mechanisms involving 
      growth factors recognized by receptors with either serine/threonine or tyrosine 
      kinase activity. Two members of the epidermal growth factor (EGF) family and 
      their respective tyrosine kinase receptors appear to play key roles in this 
      regulatory process. Transforming growth factor-alpha (TGFalpha) and its distant 
      congeners, the neuregulins (NRGs), are produced in hypothalamic astrocytes. They 
      stimulate LHRH secretion indirectly, via activation of erbB-1/erbB-2 and 
      erbB-4/erbB-2 receptor complexes also located on astrocytes. Activation of these 
      receptors leads to release of prostaglandin E(2) (PGE(2)), which then binds to 
      specific receptors on LHRH neurons to elicit LHRH secretion. Gonadal steroids 
      facilitate this glia-to-neuron communication process by acting at three different 
      steps along the signaling pathway. They (a) increase astrocytic gene expression 
      of at least one of the EGF-related ligands (TGFalpha), (b) increase expression of 
      at least two of the receptors (erbB-4 and erbB-2), and (c) enhance the LHRH 
      response to PGE(2) by up-regulating in LHRH neurons the expression of specific 
      PGE(2) receptor isoforms. Focal overexpression of TGFalpha in either the median 
      eminence or preoptic area of the hypothalamus accelerates puberty. Conversely, 
      blockade of either TGFalpha or NRG hypothalamic actions delays the process. Thus, 
      both TGFalpha and NRGs appear to be physiological components of the central 
      neuroendocrine mechanism controlling the initiation of female puberty. By 
      facilitating growth factor signaling pathways in the hypothalamus, ovarian 
      steroids accelerate the pace and progression of the pubertal process.
CI  - Copyright 1999 John Wiley & Sons, Inc.
FAU - Ojeda, S R
AU  - Ojeda SR
AD  - Division of Neuroscience, Oregon Regional Primate Research Center/Oregon Health 
      Sciences University, 505 N.W. 185th Avenue, Beaverton, Oregon 97006, USA.
FAU - Ma, Y J
AU  - Ma YJ
LA  - eng
GR  - HD25123/HD/NICHD NIH HHS/United States
GR  - P30 HD18185/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  - United States
TA  - J Neurobiol
JT  - Journal of neurobiology
JID - 0213640
RN  - 0 (Gonadal Steroid Hormones)
SB  - IM
MH  - Animals
MH  - Cell Communication/physiology
MH  - Gonadal Steroid Hormones/*physiology
MH  - Humans
MH  - Neuroglia/*physiology
MH  - Neurons/*physiology
MH  - Neurosecretory Systems/*physiology
MH  - Puberty/*physiology
MH  - Sexual Maturation/*physiology
RF  - 95
EDAT- 1999/08/24 00:00
MHDA- 1999/08/24 00:01
CRDT- 1999/08/24 00:00
PHST- 1999/08/24 00:00 [pubmed]
PHST- 1999/08/24 00:01 [medline]
PHST- 1999/08/24 00:00 [entrez]
AID - 10.1002/(SICI)1097-4695(19990915)40:4<528::AID-NEU9>3.0.CO;2-V [pii]
AID - 10.1002/(sici)1097-4695(19990915)40:4<528::aid-neu9>3.0.co;2-v [doi]
PST - ppublish
SO  - J Neurobiol. 1999 Sep 15;40(4):528-40. doi: 
      10.1002/(sici)1097-4695(19990915)40:4<528::aid-neu9>3.0.co;2-v.