1992
DOI: 10.1016/0169-328x(92)90146-3
|View full text |Cite
|
Sign up to set email alerts
|

Regulation of aromatase cytochrome P-450 (estrogen synthetase) transcripts in the quail brain by testosterone

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2

Citation Types

1
52
1
2

Year Published

1996
1996
2006
2006

Publication Types

Select...
9

Relationship

3
6

Authors

Journals

citations
Cited by 94 publications
(56 citation statements)
references
References 28 publications
1
52
1
2
Order By: Relevance
“…These observations imply that locally produced estrogens may influence sensory processing at the level of the spinal dorsal horn and may explain how gonadal hormones in males exert their pain-modulating function. Furthermore, Evrard and collaborators found that, in the spinal cord, aromatase expression is not controlled by testosterone, contrary to what is the case in many other parts of the central nervous system (Harada et al, 1992;Roselli et al, 1998), opening the possibility that, instead, neural stimuli may regulate its activity. It has been shown in cultured diencephalic neurons from fetal mice that several peptide neurotransmitters, such as substance P, and ␣-adrenergic agonists increase aromatase expression through the activation of protein kinases (Abe-Dohmae et al, 1996), and recent work suggests that activation of glutamate receptors inhibits aromatase activity in hypothalamic neurons by calcium-dependent phosphorylation (Balthazart et al, 1999).…”
mentioning
confidence: 85%
“…These observations imply that locally produced estrogens may influence sensory processing at the level of the spinal dorsal horn and may explain how gonadal hormones in males exert their pain-modulating function. Furthermore, Evrard and collaborators found that, in the spinal cord, aromatase expression is not controlled by testosterone, contrary to what is the case in many other parts of the central nervous system (Harada et al, 1992;Roselli et al, 1998), opening the possibility that, instead, neural stimuli may regulate its activity. It has been shown in cultured diencephalic neurons from fetal mice that several peptide neurotransmitters, such as substance P, and ␣-adrenergic agonists increase aromatase expression through the activation of protein kinases (Abe-Dohmae et al, 1996), and recent work suggests that activation of glutamate receptors inhibits aromatase activity in hypothalamic neurons by calcium-dependent phosphorylation (Balthazart et al, 1999).…”
mentioning
confidence: 85%
“…It is generally accepted that the aromatase enzyme depends on the androgenic status of animals. Thus, castration decreases aromatase activity and mRNA levels, whereas T treatment restores them (Harada et al 1992, Abdelgadir et al 1994. Cytochrome P450 aromatase has been found in neurons from the cerebral cortex of neonatal rats (Zwain & Yen 1999).…”
Section: Discussionmentioning
confidence: 99%
“…AR are colocalized in aromatase-positive cells but no estrogen receptor-α (ERα) can usually be detected in most of the cells expressing this enzyme in the POM or BST, although ERα are present in many adjacent cells of the same nuclei. It has been hypothesized that the effects of estrogens on aromatase transcription are mediated transynaptically [79]while androgens may act directly on the aromatase gene [80, 81, 82, 83]. Studies undertaken with in vitro systems have shown that the interactions of SRC-1 with ERα are stronger than with AR but the relative importance of this coactivator for the modulation of both estrogen and androgen receptor action in vivo remains to be determined.…”
Section: Discussionmentioning
confidence: 99%