PMID- 16454803
OWN - NLM
STAT- MEDLINE
DCOM- 20060526
LR  - 20131121
IS  - 0953-8194 (Print)
IS  - 0953-8194 (Linking)
VI  - 18
IP  - 3
DP  - 2006 Mar
TI  - Rapid neural Fos responses to oestradiol in oestrogen receptor alphabeta double 
      knockout mice.
PG  - 195-202
AB  - The standard mode of action for oestradiol is via activation of nuclear oestrogen 
      receptors (ERs), which initiate DNA transcription leading to protein formation. 
      In the present study, we examined the rapid and potentially ER-independent action 
      of oestradiol using Fos as a marker of neural activity. We assessed Fos 
      immunoreactivity (ir) in brains of mice with functional versus nonfunctional ERs. 
      Fos-ir was compared in brains of control mice that did and did not receive 
      oestradiol treatment prior to sacrifice, and cell numbers in the preoptic area 
      (POA), ventromedial nucleus of the hypothalamus (VMH), area 2 of cingulate cortex 
      (CG2), granular layer of accessory olfactory bulb (Gr-AOB), olivary pretectal 
      nucleus (OPT) and pyramidal layer of field CA3 of hippocampus (Py-CA3) were 
      increased 90 min after oestradiol treatment. By contrast, in brains of double 
      oestrogen receptor alphabeta knockout (ERalphabetaKO) female mice, no change in 
      Fos-ir was noted after oestradiol treatment in the POA, VMH, Gr-AOB or Py-CA3, 
      suggesting that these responses to oestradiol depend on ERalpha and/or ERbeta. 
      However, Fos-ir was induced by oestradiol in the OPT and CG2 in ERalphabetaKO 
      mice. These regions do not contain ERalpha-ir in control brains. In ERalphabetaKO 
      brains as well, ERalpha-ir was absent, suggesting that the mutant ERalpha (E1) 
      present in ERalphaKO brain is also absent in these regions. We speculate that 
      oestradiol has rapid effects in the OPT and CG2 via a novel mechanism that does 
      not require either classic oestrogen receptor.
FAU - Dominguez-Salazar, E
AU  - Dominguez-Salazar E
AD  - Department of Biochemistry and Molecular Genetics, University of Virginia School 
      of Medicine, Charlottesville, VA 22908, USA.
FAU - Shetty, S
AU  - Shetty S
FAU - Rissman, E F
AU  - Rissman EF
LA  - eng
GR  - K02 MH01349/MH/NIMH NIH HHS/United States
GR  - R01MH57759/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PL  - United States
TA  - J Neuroendocrinol
JT  - Journal of neuroendocrinology
JID - 8913461
RN  - 0 (Estrogen Receptor alpha)
RN  - 0 (Estrogen Receptor beta)
RN  - 0 (Proto-Oncogene Proteins c-fos)
RN  - 4TI98Z838E (Estradiol)
SB  - IM
MH  - Animals
MH  - Brain/drug effects/metabolism
MH  - Estradiol/*pharmacology
MH  - Estrogen Receptor alpha/genetics/*physiology
MH  - Estrogen Receptor beta/genetics/*physiology
MH  - Female
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Proto-Oncogene Proteins c-fos/*metabolism
EDAT- 2006/02/04 09:00
MHDA- 2006/05/27 09:00
CRDT- 2006/02/04 09:00
PHST- 2006/02/04 09:00 [pubmed]
PHST- 2006/05/27 09:00 [medline]
PHST- 2006/02/04 09:00 [entrez]
AID - JNE1408 [pii]
AID - 10.1111/j.1365-2826.2005.01408.x [doi]
PST - ppublish
SO  - J Neuroendocrinol. 2006 Mar;18(3):195-202. doi: 10.1111/j.1365-2826.2005.01408.x.