Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-1-26
pubmed:abstractText
Elevated amygdala activity and increased responsiveness of the hypothalamic-pituitary-adrenal axis have been observed in irritable bowel syndrome (IBS) patients. Recently, we demonstrated that corticosterone (Cort) placed on the amygdala induced anxiety-like behavior coupled with decreased thresholds for visceral and somatic pain in rats. Moreover, these studies suggested that the effects of Cort were dependent on both the glucocorticoid receptor (GR) and mineralocorticoid receptor (MR); however, the specific contributions of these receptors to the interaction between corticosteroids and the amygdala are still unclear. In the present study, we sought to define the distinct roles of amygdaloid GR and MR in anxiety-like behavior, visceral sensitivity, and somatic sensitivity through selective pharmacological activation. Male Fischer 344 rats received bilateral implants on the dorsal margin of the central amygdala containing the GR agonist dexamethasone (Dex), the MR agonist aldosterone (Aldo), or cholesterol as a control. Our results showed that GR or MR activation significantly reduced open arm exploration on the elevated plus maze, a measure of anxiety-like behavior. Aldo increased the number of abdominal muscle contractions in response to all levels of colorectal distension (CRD). In contrast, Dex only increased visceral sensitivity at noxious levels of CRD. Furthermore, GR but not MR activation reduced somatic pain thresholds measured by the mechanical force required to elicit hindlimb withdrawal. In summary, GR and MR mediated-mechanisms induce anxiety and visceral hypersensitivity, whereas somatic sensitivity involves only GR, suggesting that corticosteroids may enhance visceral and somatic sensation via divergent processes originating in the amygdala and involving specific steroid receptor mechanisms.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1522-1547
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
298
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G295-303
pubmed:meshHeading
pubmed-meshheading:19875699-Aldosterone, pubmed-meshheading:19875699-Amygdala, pubmed-meshheading:19875699-Animals, pubmed-meshheading:19875699-Anxiety, pubmed-meshheading:19875699-Behavior, Animal, pubmed-meshheading:19875699-Dexamethasone, pubmed-meshheading:19875699-Glucocorticoids, pubmed-meshheading:19875699-Hypothalamo-Hypophyseal System, pubmed-meshheading:19875699-Irritable Bowel Syndrome, pubmed-meshheading:19875699-Male, pubmed-meshheading:19875699-Motor Activity, pubmed-meshheading:19875699-Nociceptors, pubmed-meshheading:19875699-Pain, pubmed-meshheading:19875699-Pain Threshold, pubmed-meshheading:19875699-Pituitary-Adrenal System, pubmed-meshheading:19875699-Rats, pubmed-meshheading:19875699-Rats, Inbred F344, pubmed-meshheading:19875699-Receptors, Glucocorticoid, pubmed-meshheading:19875699-Receptors, Mineralocorticoid
pubmed:year
2010
pubmed:articleTitle
Divergent effects of amygdala glucocorticoid and mineralocorticoid receptors in the regulation of visceral and somatic pain.
pubmed:affiliation
Veterans Affairs Medical Center, Oklahoma Center for Neuroscience, University of Oklahoma Health Sciences Center, 921 NE 13 St., Oklahoma City, OK 73104, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S.