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Inhibition by Lipopolysaccharide of Naloxone‐Induced Luteinising Hormone Secretion Is Accompanied by Increases in Corticotropin‐Releasing Factor Immunoreactivity in Hypothalamic Paraventricular Neurones in Female Rats
Author(s) -
He D.,
Akema T.
Publication year - 2005
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1111/j.1365-2826.2005.01275.x
Subject(s) - endocrinology , medicine , (+) naloxone , hypothalamus , secretion , corticotropin releasing hormone , lipopolysaccharide , chemistry , antagonist , receptor
We have recently reported that lipopolysaccharide (LPS), a bacterial endotoxin, inhibits steroid‐induced as well as naloxone‐induced luteinising hormone (LH) secretion in ovariectomised oestrogen‐primed rats. In the present study, we examined whether corticotropin‐releasing factor (CRF) may be involved in the LPS‐induced inhibition of LH secretion. Unanaesthetised rats were treated with an intravenous (i.v.) injection of LPS (10 µg) or saline, followed by an i.v. injection of naloxone (20 mg/kg). After sequential blood samples were collected for determination of serum LH concentrations, the brains were fixed and CRF‐immunoreactivity was examined histochemically. In control rats receiving saline injections, only a small number of CRF‐immunoreactive (ir) cells were found in the parvocellular portion of the hypothalamic paraventricular nucleus (PVN), and naloxone significantly increased serum LH concentrations within 10 min. By contrast, in LPS‐treated rats, the number of CRF‐ir cells was significantly greater than that in control rats, and the effect of naloxone was completely abolished. In a separate experiment, an intracerebroventricular injection of 5 µg CRF inhibited naloxone‐induced LH release, mimicking the effect of LPS. These results suggest that LPS stimulates production of CRF in PVN neurones, which in turn inhibits LH secretion without opioidergic mediation.