Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1996-6-21
pubmed:abstractText
As the GnRH-induced secretion of gonadotropins is critically dependent upon an increase in the intracellular calcium ion concentration ([Ca2+]i) and modulated by gonadal factors, the effects of gonadal steroids on the pattern of calcium mobilization in single gonadotrophs of the male rat were examined using the fluorescent Ca2+ indicator fura-2/AM. In cells from intact rats, low concentrations of GnRH induce repetitive oscillations in [Ca2+]i, whereas spike-plateau responses are observed at higher concentrations in single gonadotrophs. After castration, there was a significant change in the relationship between the GnRH concentration and the changes in [Ca2+]i. Increasing concentrations of GnRH (to 1 micron) generate fewer spike-plateau responses in gonadotrophs from castrate rats, with oscillatory responses predominating. This change develops with time after castration, with the proportion of cells oscillating in response to 100 nM GnRH peaking by 7 days. This effect of castration on GnRH-induced [Ca2+]i signals was reversed by treatment with testosterone propionate (100 microgram/100 g BW-day). Castration-induced decreases in serum testosterone, seminal vesicle, and prostate weights and increases in serum LH concentration were also corrected by testosterone propionate treatment. These findings demonstrate that testosterone regulates GnRH-stimulated Ca2+ signals in gonadotrophs and suggest that gonadal steroids exert a regulatory role in the secretion of gonadotropins at the level of Ca2+ mobilization.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
137
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1299-305
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Testosterone regulates gonadotropin-releasing hormone-induced calcium signals in male rat gonadotrophs.
pubmed:affiliation
Department of Physiology, Monash University, Clayton, Victoria 3168, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't