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Nitric oxide, interleukin and prostaglandin interactions affecting the magnocellular system
Joan Y Summy-Long1, Vuong Bui, Shelley Gestl
1Department of Pharmacology-MCH108, The Pennsylvania State University, The Milton S. Hershey Medical Center, P.O. Box 850, Hershey, PA 17033, USA. jsl2@psu.edu
Brain Research
|May 22, 2002
Summary
Nitric oxide (NO) normally inhibits oxytocin (OT) release. Inhibiting NO increases OT, an effect reduced by blocking cyclo-oxygenase (COX) or histamine receptors, suggesting NO regulates OT via these pathways.
Area of Science:
- Neuroendocrinology
- Cellular signaling
Background:
- Magnocellular neurons utilize excitatory histaminergic pathways.
- These neurons express neuronal nitric oxide synthase (NOS), interleukin-1beta (IL-1beta), and cyclo-oxygenase (COX).
Purpose of the Study:
- To investigate the role of nitric oxide (NO) in regulating oxytocin (OT) release.
- To elucidate the mechanisms by which NO interacts with COX, histamine, and IL-1beta in controlling OT secretion.
Main Methods:
- Intracerebroventricular administration of N(G)-nitro-L-arginine methyl ester (L-NAME) to inhibit NO synthase activity in rats.
- Administration of indomethacin (COX inhibitor), pyrilamine (H1 antagonist), and cimetidine (H2 antagonist) to assess their effects on L-NAME-induced OT release.
- Investigating the impact of centrally administered IL-1beta and prostaglandins (PGE2, PGD2) on OT and vasopressin levels.
Main Results:
- Inhibition of NO synthase by L-NAME increased plasma OT concentrations.
- This L-NAME-induced OT increase was attenuated by indomethacin, pyrilamine, and cimetidine.
- Centrally administered IL-1beta-induced OT secretion was blocked by indomethacin, but not naloxone.
- PGE2 and PGD2 stimulated OT release, with PGD2 also affecting vasopressin levels.
Conclusions:
- NO inhibits OT release through COX-dependent and histamine-mediated pathways.
- NO may also regulate IL-1beta-stimulated OT release via a COX-dependent mechanism.
- These interactions between NO, cytokines, and histamine are crucial for managing stress-induced neuroendocrine responses.