PMID- 9380280
OWN - NLM
STAT- MEDLINE
DCOM- 19971107
LR  - 20180214
IS  - 0028-3835 (Print)
IS  - 0028-3835 (Linking)
VI  - 66
IP  - 3
DP  - 1997 Sep
TI  - Characterization of the effect of Mycoplasma fermentans on the 
      hypothalamo-pituitary-adrenal axis.
PG  - 221-8
AB  - The mechanisms involved in the activation of the hypothalamus-pituitary-adrenal 
      axis after administration of Mycoplasma fermentans were examined. Male rats were 
      injected intracerebroventricularly (i.c.v.) with heat-inactivated M. fermentas (6 
      micrograms protein/10 microliters/rat) or vehicle and were killed 2 h later. M. 
      fermentans caused a significant depletion of corticotropin releasing hormone 
      (CRH-41) content in the median eminence (ME), and elevation of serum ACTH and 
      corticosterone (CS) levels, compared to control levels. Pretreatment with 
      dexamethasone (DEX, 40 micrograms/kg) markedly inhibited M. fermentans-induced 
      depletion of ME CRH-41 and the increase in serum ACTH and CS. Injection of the 
      type II corticosteroid receptor antagonist RU-38486, but not the type 1 
      antagonist RU-28318, enhanced the adrenocortical response and completely 
      abolished the inhibitory effect of DEX following M. fermentans. Injection of the 
      catecholamine neurotoxin 6-hydroxydopamine into the ventral noradrenergic bundle, 
      which significantly depleted hypothalamic norepinephrine content, or i.c.v. 
      injection of the specific alpha 1-adrenergic receptor antagonist prazosin failed 
      to affect the adrenocortical response to M. fermentans. In contrast, these agents 
      markedly inhibited the adrenocortical response following i.c.v. injection of 
      interleukin-1. I.c.v. administration of M. fermentans caused a significant 
      elevation of hypothalamic levels of tumor necrosis factor-alpha (TNF alpha), 
      determined by both bioassay and immunoassay. In rats treated with pentoxifylline, 
      an inhibitor of TNF alpha synthesis, the adrenocortical response to M. fermentans 
      was markedly inhibited. These findings suggest that: (1) M. fermentans-induced 
      activation of the pituitary-adrenal axis, and the inhibitory effect of DEX on 
      this response, are mediated by a reduction of CRH-41 release from the ME. (2) The 
      feedback exerted by glucocorticoids is mediated by type II corticosteroid 
      receptors. (3) In contrast to the adrenocortical response to interleukin-1 beta, 
      the central noradrenergic system does not have an important role in mediating the 
      adrenocortical response to M. fermentans. (4) Hypothalamic TNF alpha production 
      is probably involved in mediating the adrenocortical activation following M. 
      fermentans.
FAU - Wohlman, A
AU  - Wohlman A
AD  - Department of Neurology, Hadassah University Hospital, Jerusalem, Israel.
FAU - Gallily, R
AU  - Gallily R
FAU - Yirmiya, R
AU  - Yirmiya R
FAU - Weidenfeld, J
AU  - Weidenfeld J
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Switzerland
TA  - Neuroendocrinology
JT  - Neuroendocrinology
JID - 0035665
RN  - 0 (Adrenergic alpha-Antagonists)
RN  - 0 (Neurotoxins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 8HW4YBZ748 (Oxidopamine)
RN  - 9015-71-8 (Corticotropin-Releasing Hormone)
RN  - XM03YJ541D (Prazosin)
SB  - IM
MH  - Adrenergic alpha-Antagonists/pharmacology
MH  - Animals
MH  - Corticotropin-Releasing Hormone/*physiology
MH  - Feedback
MH  - Hypothalamo-Hypophyseal System/*physiology
MH  - Injections, Intraventricular
MH  - Male
MH  - Median Eminence/metabolism
MH  - Mycoplasma/*physiology
MH  - Neurotoxins
MH  - Oxidopamine
MH  - Pituitary-Adrenal System/*physiology
MH  - Prazosin/pharmacology
MH  - Rats
MH  - Tumor Necrosis Factor-alpha/physiology
EDAT- 1997/10/06 00:00
MHDA- 1997/10/06 00:01
CRDT- 1997/10/06 00:00
PHST- 1997/10/06 00:00 [pubmed]
PHST- 1997/10/06 00:01 [medline]
PHST- 1997/10/06 00:00 [entrez]
AID - 10.1159/000127241 [doi]
PST - ppublish
SO  - Neuroendocrinology. 1997 Sep;66(3):221-8. doi: 10.1159/000127241.