Abstract：
:This study demonstrates that a single subcutaneous injection of gonadotrophin-releasing hormone (GnRH) (60 ng) to GnRH-deficient (hpg) male mice causes a doubling of pituitary GnRH receptors (GnRH-R). No change in GnRH-R occurs during the time of LH release (15-60 min) or up until 4 h post-GnRH. Between 4 and 12 h there is a progressive increase in GnRH-R, which is still apparent 24 h later. No induction of GnRH-R occurs after the same treatment of intact adult normal mice. The same degree of GnRH-R induction occurs 12 h after a single GnRH injection (60 ng) to orchidectomized hpg male mice, indicating that this effect is mediated by a direct action of GnRH on the pituitary gonadotroph, rather than being secondary to stimulation of some gonadal product. Homologous ligand GnRH-R induction in hpg mouse pituitaries in vivo is prevented by prior treatment with cycloheximide, a non-specific protein synthesis inhibitor. Cycloheximide alone had no effect on GnRH-R in normal male mice but when combined with GnRH caused a 40% depletion of receptors, implying ligand-induced receptor loss without subsequent replenishment. The similarity between the extent, time-course, and dependence on protein synthesis of GnRH induction of its own receptors in vivo and in cultured pituitary cells in vitro indicates that the hpg mouse pituitary behaves like an in vivo pituitary cell culture system in this respect. Similarity of data derived from this in vivo model provides direct support for the view that in vitro studies on the cellular mechanism of GnRH action can be physiologically relevant to the intact animal.
journal_name
Mol Cell Endocrinoljournal_title
Molecular and cellular endocrinologyauthors
Detta A,Naik SI,Charlton HM,Young LS,Clayton RNdoi
10.1016/0303-7207(84)90045-5subject
Has Abstractpub_date
1984-09-01 00:00:00pages
139-44issue
2eissn
0303-7207issn
1872-8057pii
0303-7207(84)90045-5journal_volume
37pub_type
杂志文章abstract：:We have localized four transcription initiation sites in the human insulin-like growth factor-I (IGF-I) gene. Two transcription start sites were identified which result in a longer and shorter version of the leader derived from the known exon 1 of the IGF-I gene. Transcription starting at the upstream transcription in...
journal_title：Molecular and cellular endocrinology
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更新日期：1991-06-01 00:00:00
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更新日期：1994-09-01 00:00:00
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journal_title：Molecular and cellular endocrinology
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journal_title：Molecular and cellular endocrinology
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更新日期：1988-02-01 00:00:00
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更新日期：2002-11-29 00:00:00
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更新日期：2008-05-14 00:00:00
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doi：10.1016/j.mce.2009.12.027
更新日期：2010-04-12 00:00:00
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journal_title：Molecular and cellular endocrinology
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journal_title：Molecular and cellular endocrinology
pub_type： 杂志文章
doi：10.1016/0303-7207(92)90260-d
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journal_title：Molecular and cellular endocrinology
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更新日期：2016-01-15 00:00:00
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更新日期：1997-03-14 00:00:00
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pub_type： 杂志文章,评审
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更新日期：2009-11-27 00:00:00
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journal_title：Molecular and cellular endocrinology
pub_type： 杂志文章
doi：10.1016/j.mce.2021.111179
更新日期：2021-01-27 00:00:00
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journal_title：Molecular and cellular endocrinology
pub_type： 杂志文章
doi：10.1016/0303-7207(93)90061-n
更新日期：1993-07-01 00:00:00
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pub_type： 杂志文章
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更新日期：2002-02-25 00:00:00
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journal_title：Molecular and cellular endocrinology
pub_type： 杂志文章
doi：10.1016/0303-7207(95)03633-i
更新日期：1995-09-22 00:00:00
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journal_title：Molecular and cellular endocrinology
pub_type： 杂志文章
doi：10.1016/0303-7207(91)90263-r
更新日期：1991-04-01 00:00:00
abstract：:Inhibin is a member of the TGF-beta superfamily of growth and differentiation factors and a tumor suppressor. Consistent with the tumor suppressive function of the inhibin alpha subunit in prostate cancer, we reported a loss of gene expression due to DNA hypermethylation and loss of heterozygosity (LOH) as well as dow...
journal_title：Molecular and cellular endocrinology
pub_type： 杂志文章
doi：10.1016/j.mce.2004.02.015
更新日期：2004-10-15 00:00:00
