PMID- 15664786
OWN - NLM
STAT- MEDLINE
DCOM- 20050428
LR  - 20131121
IS  - 0889-1591 (Print)
IS  - 0889-1591 (Linking)
VI  - 19
IP  - 2
DP  - 2005 Mar
TI  - The role of central corticotropin-releasing hormone in the anorexic and endocrine 
      effects of the bacterial T cell superantigen, Staphylococcal enterotoxin A.
PG  - 138-46
AB  - Bacterial superantigens, such as the staphylococcal enterotoxins, exert a strong 
      capacity for in vivo stimulation of T cell proliferation and cytokine production. 
      Previously, staphylococcal enterotoxin A (SEA) was shown to induce an anorexic 
      effect under novel contextual conditions of testing, and produced an increase in 
      plasma ACTH and corticosterone levels in C57BL/6J mice. In the present study, the 
      role of corticotropin releasing hormone (CRH) in promoting these effects of SEA 
      was addressed via intracerebroventricular (icv) administration of alpha-helical 
      CRH(9-41) ((alpha)hCRH), a non-selective CRH receptor antagonist, and 
      astressin-2B, a selective CRH receptor 2 antagonist. The efficacy of (alpha)hCRH 
      and astressin-2B in blocking anorexic responses to CRH and urocortin under the 
      current conditions of testing was first confirmed. Subsequently, it was found 
      that (alpha)hCRH (20 microg icv), but not astressin-2B (10 and 25 microg icv), 
      significantly attenuated the anorexia induced by SEA. This suggested that central 
      CRH is involved in mediating the anorexia induced by SEA, but potentially through 
      CRH receptor 1. Additional results revealed that plasma ACTH stimulation in 
      response to SEA was not significantly attenuated by either antagonist 
      administered icv. However, the plasma corticosterone elevation showed a modest, 
      but significant, attenuation in SEA challenged mice given (alpha)hCRH. These data 
      suggest a possible influence of central CRH on adrenocorticoid activity 
      subsequent to SEA challenge. More importantly, it appears that central activation 
      of CRH receptors is a consequence of SEA challenge, and this likely contributes 
      to its anorexic effects.
FAU - Kaneta, Takehiro
AU  - Kaneta T
AD  - Department of Psychology, Biopsychology and Behavioral Neuroscience Program, 
      Rutgers University, 152 Frelinghuysen Road, Piscataway, NJ 08855, USA.
FAU - Kusnecov, Alexander W
AU  - Kusnecov AW
LA  - eng
GR  - DA141186/DA/NIDA NIH HHS/United States
GR  - MH60706/MH/NIMH NIH HHS/United States
GR  - P30 ES05022/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Brain Behav Immun
JT  - Brain, behavior, and immunity
JID - 8800478
RN  - 0 (Enterotoxins)
RN  - 0 (Hormone Antagonists)
RN  - 0 (Interferon Inducers)
RN  - 0 (Peptide Fragments)
RN  - 0 (Receptors, Corticotropin-Releasing Hormone)
RN  - 37337-57-8 (enterotoxin A, Staphylococcal)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
RN  - 96118-75-1 (corticotropin releasing hormone (9-41))
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Adrenocorticotropic Hormone/blood
MH  - Animals
MH  - Anorexia/chemically induced/*immunology/physiopathology
MH  - Appetite/drug effects/immunology
MH  - Corticosterone/blood
MH  - Corticotropin-Releasing Hormone/pharmacology/*physiology
MH  - Eating/drug effects/immunology
MH  - Enterotoxins/*pharmacology
MH  - Hormone Antagonists/pharmacology
MH  - Injections, Intraventricular
MH  - Interferon Inducers/*pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Peptide Fragments/pharmacology
MH  - Receptors, Corticotropin-Releasing Hormone/physiology
EDAT- 2005/01/25 09:00
MHDA- 2005/04/29 09:00
CRDT- 2005/01/25 09:00
PHST- 2004/02/11 00:00 [received]
PHST- 2004/05/25 00:00 [revised]
PHST- 2004/06/14 00:00 [accepted]
PHST- 2005/01/25 09:00 [pubmed]
PHST- 2005/04/29 09:00 [medline]
PHST- 2005/01/25 09:00 [entrez]
AID - S0889-1591(04)00075-3 [pii]
AID - 10.1016/j.bbi.2004.06.002 [doi]
PST - ppublish
SO  - Brain Behav Immun. 2005 Mar;19(2):138-46. doi: 10.1016/j.bbi.2004.06.002.