PMID- 17480015
OWN - NLM
STAT- MEDLINE
DCOM- 20070815
LR  - 20220409
IS  - 0021-9967 (Print)
IS  - 1096-9861 (Electronic)
IS  - 0021-9967 (Linking)
VI  - 503
IP  - 1
DP  - 2007 Jul 1
TI  - Distribution and localization patterns of estrogen receptor-beta and insulin-like 
      growth factor-1 receptors in neurons and glial cells of the female rat substantia 
      nigra: localization of ERbeta and IGF-1R in substantia nigra.
PG  - 198-208
AB  - Although several studies have focused on the neuroprotective effects of estrogen 
      (E2) on stroke, there have been tantalizing reports on the potential 
      neuroprotective role of E2 in degenerative neuronal diseases such as Alzheimer's 
      and Parkinson's (PD). In animal models of PD, E2 protects the nigrostriatal 
      dopaminergic (DA) system against neurotoxins. However, little is known about the 
      cellular and molecular mechanism(s) involved by which E2 elicits its 
      neuroprotective effects on the nigrostriatal DA system. A preferred mechanism for 
      neuroprotection is the interaction of E2 with specific neuroprotective growth 
      factors and receptors. One such neuroprotective factor/receptor system is 
      insulin-like growth factor-1 (IGF-1). E2 neuroprotective effects in the 
      substantia nigra (SN) DA system have been shown to be dependent on IGF-1. To 
      determine whether E2 also interacts with the IGF-1 receptor (IGF-1R) and to 
      determine the cellular localization of estrogen receptor (ER) and IGF-1R, we 
      compared the distribution of ER and IGF-1R in the SN. Stereological measurements 
      revealed that 40% of the subpopulation of tyrosine hydroxylase-immunoreactive 
      (TH-ir) SN pars compacta (SNpc) DA neurons are immunoreactive for estrogen 
      receptor-beta (ERbeta). No immunolabeling for ERalpha was observed. In situ 
      hybridization and immunocytochemistry studies confirmed the expression of IGF-1R 
      mRNA and revealed that almost all TH-ir SNpc DA neurons were immunoreactive for 
      IGF-1R, respectively. Moreover, one-third of glial fibrillary acidic protein 
      (GFAP-ir) cells in the SN were ERbeta-ir, and 67% of GFAP-ir cells expressed 
      IGF-1R-ir. Therefore, the localization of ERbeta and IGF-1R on SNpc DA neurons 
      and astrocytes suggests a modulatory role of E2 on IGF-1R, and this modulation 
      may affect neuroprotection.
FAU - Quesada, Arnulfo
AU  - Quesada A
AD  - Department of Neurobiology, Laboratory of Neuroendocrinology of the Brain 
      Research Institute, David Geffen School of Medicine at the University of 
      California Los Angeles, Los Angeles, CA 90095-1763, USA. aquesada@mednet.ucla.edu
FAU - Romeo, Horacio E
AU  - Romeo HE
FAU - Micevych, Paul
AU  - Micevych P
LA  - eng
GR  - R21 DE016063/DE/NIDCR NIH HHS/United States
GR  - R21 DE016063-02/DE/NIDCR NIH HHS/United States
GR  - DE016063-01/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Comp Neurol
JT  - The Journal of comparative neurology
JID - 0406041
RN  - 0 (Estrogen Receptor beta)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
RN  - EC 2.7.10.1 (Receptor, IGF Type 1)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Dopamine/metabolism
MH  - Estrogen Receptor beta/*metabolism
MH  - Female
MH  - Fluorescent Antibody Technique
MH  - Glial Fibrillary Acidic Protein/metabolism
MH  - Neuroglia/*metabolism
MH  - Neurons/*metabolism
MH  - Rats
MH  - Rats, Long-Evans
MH  - Receptor, IGF Type 1/*metabolism
MH  - Substantia Nigra/cytology/*metabolism
MH  - Tyrosine 3-Monooxygenase/metabolism
PMC - PMC2907103
MID - NIHMS216872
EDAT- 2007/05/08 09:00
MHDA- 2007/08/19 09:00
PMCR- 2010/07/20
CRDT- 2007/05/08 09:00
PHST- 2007/05/08 09:00 [pubmed]
PHST- 2007/08/19 09:00 [medline]
PHST- 2007/05/08 09:00 [entrez]
PHST- 2010/07/20 00:00 [pmc-release]
AID - 10.1002/cne.21358 [doi]
PST - ppublish
SO  - J Comp Neurol. 2007 Jul 1;503(1):198-208. doi: 10.1002/cne.21358.