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Volume 17, Number 23,
Issue of December 1, 1997
pp. 9145-9156
Estradiol Enhances Prostaglandin E2 Receptor Gene
Expression in Luteinizing Hormone-Releasing Hormone (LHRH) Neurons and
Facilitates the LHRH Response to PGE2 by Activating a
Glia-to-Neuron Signaling Pathway
Received June 3, 1997; revised Sept. 8, 1997; accepted Sept. 18, 1997.
Florence Rage,
Byung Ju Lee,
Ying J. Ma, and
Sergio R. Ojeda
Division of Neuroscience, Oregon Regional Primate Research
Center-Oregon Health Sciences University, Beaverton, Oregon 97006
Prostaglandin E2 (PGE2) mediates the
stimulatory effect of norepinephrine (NE) on the secretion of
luteinizing hormone-releasing hormone (LHRH), the neuropeptide
controlling reproductive function. In rodents, this facilitatory effect
requires previous exposure to estradiol, suggesting that the steroid
affects downstream components in the cascade that leads to
PGE2-induced LHRH release. Because astroglia are the
predominant cell type contacting LHRH-secreting nerve terminals, we
investigated the involvement of hypothalamic astrocytes in the
estradiol facilitation of PGE2-induced LHRH release. A
subpopulation of LHRH neurons was found to express the mRNA encoding
the PGE2 receptor subtype EP1-R, which is coupled to
calcium mobilization. The LHRH-producing cell line GT1-1 also contains
EP1-R mRNA and, to a lesser extent, the three alternatively spliced
forms of EP3-R mRNA ( ,  , and  ) that encode receptors linked to
inhibition and stimulation of cAMP formation. Hypothalamic astrocytes
treated with estradiol produced a conditioned medium that when applied
to GT1-1 cells resulted in a selective upregulation of EP1-R and
EP3-R mRNAs. The conditioned medium also enhanced the LHRH
response to EP1-R and EP3-R agonists and the cAMP response to EP3-R
activation. Thus, one mechanism by which estradiol facilitates the
effect of neurotransmitters acting via PGE2 to stimulate
LHRH release is by enhancing the glial production of substances that upregulate PGE2 receptors on LHRH neurons. The existence of
such a mechanism underscores the emerging importance of glial-neuronal communication in the control of brain neurosecretory activity.
Key words:
gonadal steroids;
astrocytes;
hypothalamus;
neuropeptide
secretion;
prostaglandin receptors;
glial-neuronal interactions
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