Search Results
You are looking at 1 - 2 of 2 items for
- Author: Fiona J Thomson x
- Refine by access: All content x
Search for other papers by Francesca Spiga in
Google Scholar
PubMed
Search for other papers by Louise R Harrison in
Google Scholar
PubMed
Search for other papers by Susan A Wood in
Google Scholar
PubMed
Search for other papers by Cliona P MacSweeney in
Google Scholar
PubMed
Search for other papers by Fiona J Thomson in
Google Scholar
PubMed
Search for other papers by Mark Craighead in
Google Scholar
PubMed
Search for other papers by Morag Grassie in
Google Scholar
PubMed
Search for other papers by Stafford L Lightman in
Google Scholar
PubMed
We investigated the effect of the glucocorticoid receptor (GR) antagonist Org 34850 on fast and delayed inhibition of corticosterone secretion in response to the synthetic glucocorticoid methylprednisolone (MPL). Male rats were implanted with a catheter in the right jugular vein, for blood sampling and MPL administration, and with an s.c. cannula for Org 34850 administration. All experiments were conducted at the diurnal hormonal peak in the late afternoon. Rats were connected to an automated sampling system and blood samples were collected every 5 or 10 min. Org 34850 (10 mg/kg, s.c.) or vehicle (5% mulgofen in saline) was injected at 1630 h; 30 min later, rats received an injection of MPL (500 μg/rat, i.v.) or saline (0.1 ml/rat). We found that an acute administration of MPL rapidly decreased the basal corticosterone secretion and this effect was not prevented by acute pretreatment with Org 34850. However, blockade of GR with Org 34850 prevented delayed inhibition of MPL on corticosterone secretion measured between 4 and 12 h after MPL administration. Our data suggest an involvement of GR in modulating delayed, but not fast, inhibition induced by MPL on basal corticosterone secretion.
Search for other papers by Francesca Spiga in
Google Scholar
PubMed
Search for other papers by Louise R Harrison in
Google Scholar
PubMed
Search for other papers by Cliona P MacSweeney in
Google Scholar
PubMed
Search for other papers by Fiona J Thomson in
Google Scholar
PubMed
Search for other papers by Mark Craighead in
Google Scholar
PubMed
Search for other papers by Stafford L Lightman in
Google Scholar
PubMed
Exposure to chronic restraint (CR) modifies the hypothalamic–pituitary–adrenal (HPA) axis response to subsequent acute stressors with adaptation of the response to a homotypic and sensitization of the response to a heterotypic stressor. Since vasopressin (AVP) activity has been reported to change during chronic stress, we investigated whether this was an important factor in HPA facilitation. We therefore tested whether vasopressin 1b receptor (AVPR1B) blockade altered the ACTH and corticosterone response to heterotypic stressors following CR stress. Adult male rats were exposed to CR, single restraint, or were left undisturbed in the home cage. Twenty-four hours after the last restraint, rats were injected with either a AVPR1B antagonist (Org, 30 mg/kg, s.c.) or vehicle (5% mulgofen in saline, 0.2/kg, s.c.) and then exposed to either restraint, lipopolysaccharide (LPS) or white noise. CR resulted in the adaptation of the ACTH and corticosterone response to restraint and this effect was not prevented by pretreatment with Org. Although we found no effect of CR on LPS-induced ACTH and corticosterone secretion, both repeated and single episodes of restraint induced the sensitization of the ACTH, but not corticosterone response to acute noise. Pretreatment with Org reduced the exaggerated ACTH response to noise after both single and repeated exposure to restraint.
