PMID- 9801392
OWN - NLM
STAT- MEDLINE
DCOM- 19981211
LR  - 20191024
IS  - 0270-6474 (Print)
IS  - 1529-2401 (Electronic)
IS  - 0270-6474 (Linking)
VI  - 18
IP  - 22
DP  - 1998 Nov 15
TI  - Induction of progestin receptors by estradiol in the forebrain of estrogen 
      receptor-alpha gene-disrupted mice.
PG  - 9556-63
AB  - Mice, rats, and humans have two types of estrogen receptors, estrogen 
      receptor-alpha (ERalpha) and estrogen receptor-beta (ERbeta). Estrogen 
      receptor-alpha gene-disrupted (ERalpha-disrupted) mice bear two nonfunctional 
      copies of the ERalpha gene. This mutation blocks the synthesis of full-length 
      ERalpha, renders the animals infertile, and inhibits the induction of female 
      sexual behaviors by estradiol and progesterone. It is likely that many of the 
      processes contributing to the regulation of sexual receptivity by estradiol and 
      progesterone are compromised in ERalpha-disrupted mice. However, given the 
      importance of progesterone in the regulation of sexual receptivity and given the 
      importance of progestin receptors (PRs) in mediating the responses of females to 
      progesterone, we investigated the effects of ERalpha disruption on the induction 
      of PRs by estradiol in the forebrain. We hypothesized that estradiol would induce 
      PRs in wild-type mice but not in ERalpha-disrupted mice. Ovariectomized wild-type 
      and ERalpha-disrupted mice were implanted with either estradiol-filled capsules 
      or empty capsules for 5 d, after which their brains were processed for the 
      immunocytochemical detection of PR. Estradiol increased the number of 
      PR-immunoreactive cells in both wild-type and ERalpha-disrupted mice. The 
      residual responsiveness of ERalpha-disrupted mice to estradiol could be accounted 
      for by an ERbeta-dependent mechanism or another as yet unidentified estrogen 
      receptor; however, because ERalpha-immunoreactivity and PCR product representing 
      the 3' end of ERalpha mRNA were found in at least one PR-containing region of the 
      ERalpha-disrupted mice, an ERalpha splice variant may also mediate the induction 
      of PR-immunoreactivity in ERalpha-disrupted mice.
FAU - Moffatt, C A
AU  - Moffatt CA
AD  - Neuroscience and Behavior Program and Center for Neuroendocrine Studies, 
      University of Massachusetts, Amherst, Massachusetts 01003, USA.
FAU - Rissman, E F
AU  - Rissman EF
FAU - Shupnik, M A
AU  - Shupnik MA
FAU - Blaustein, J D
AU  - Blaustein JD
LA  - eng
GR  - MH56187/MH/NIMH NIH HHS/United States
GR  - K05-MH01212/MH/NIMH NIH HHS/United States
GR  - K02 MH001349/MH/NIMH NIH HHS/United States
GR  - F32 HD008181/HD/NICHD NIH HHS/United States
GR  - HD08181/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci
JT  - The Journal of neuroscience : the official journal of the Society for 
      Neuroscience
JID - 8102140
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Estrogen)
RN  - 0 (Receptors, Progesterone)
RN  - 4TI98Z838E (Estradiol)
SB  - IM
MH  - Animals
MH  - Brain Chemistry/drug effects
MH  - Estradiol/*pharmacology
MH  - Female
MH  - Gene Expression/physiology
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Ovariectomy
MH  - Prosencephalon/*chemistry
MH  - RNA, Messenger/analysis
MH  - Receptors, Estrogen/*genetics
MH  - Receptors, Progesterone/analysis/*genetics
MH  - Ventromedial Hypothalamic Nucleus/*chemistry
PMC - PMC6792867
EDAT- 1998/11/05 00:00
MHDA- 1998/11/05 00:01
PMCR- 1999/05/15
CRDT- 1998/11/05 00:00
PHST- 1998/11/05 00:00 [pubmed]
PHST- 1998/11/05 00:01 [medline]
PHST- 1998/11/05 00:00 [entrez]
PHST- 1999/05/15 00:00 [pmc-release]
AID - 2525 [pii]
AID - 10.1523/JNEUROSCI.18-22-09556.1998 [doi]
PST - ppublish
SO  - J Neurosci. 1998 Nov 15;18(22):9556-63. doi: 10.1523/JNEUROSCI.18-22-09556.1998.