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Immunohistochemical Analysis in the Rat Central Nervous System and Peripheral Lymph Node Tissue Sections
Published on: November 14, 2016
Evidence for the neuronal origin of immunoreactive interleukin-1 beta released by rat hypothalamic explants
G Tringali1, C Mancuso, A Mirtella
1Institute of Pharmacology, Catholic University Medical School, Rome, Italy.
Insights
Rat hypothalamic explants release interleukin-1 beta (IL-1 beta). Potassium and noradrenaline stimulate this release, which is blocked by specific ion channel inhibitors, suggesting a neuronal origin for IL-1 beta.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Interleukin-1 beta (IL-1 beta) is a key inflammatory cytokine.
- The hypothalamus plays a crucial role in regulating physiological processes.
- Neuronal release of IL-1 beta is not fully understood.
Purpose of the Study:
- To investigate the release of immunoreactive IL-1 beta (irIL-1 beta) from rat hypothalamus in vitro.
- To determine the mechanisms regulating irIL-1 beta release.
Main Methods:
- Tissue explant culture of rat hypothalamus.
- Stimulation with high potassium (KCl) and noradrenaline.
- Inhibition studies using specific ion channel blockers (omega-conotoxin, verapamil, nifedipine, tetrodotoxin, lidocaine) and receptor antagonists (propranolol, phentolamine).
Main Results:
- Rat hypothalamic explants release significant amounts of irIL-1 beta.
- K(+)-induced release is dependent on N-type calcium and Na+ channels.
- Noradrenaline enhances irIL-1 beta release via beta-adrenergic receptors.
- Involvement of verapamil and propranolol suggests a role for calcium and beta-adrenergic signaling.
Conclusions:
- Hypothalamic irIL-1 beta release is stimulated by depolarization and noradrenaline.
- The release mechanism involves voltage-gated calcium and sodium channels.
- Evidence strongly suggests that irIL-1 beta released from hypothalamic explants is of neuronal origin.
Abstract:
In this study, we have investigated the release of immunoreactive interleukin-1 beta (irIL-1 beta) from the rat hypothalamus in vitro. It was found that (1) tissue explants release sizable amounts of irIL-1 beta (ranging from 0.43 to 0.52 pg/mg of wet tissue) in 20 min incubations; (2) basal release in significantly increased by depolarization induced with 56 mM KCl; (3) K(+)-induced irIL-1 beta release is inhibited by the specific blocker of N-type calcium channels, omega-conotoxin, and by verapamil, but not by nifedipine; (4) K(+)-induced release is also inhibited by the Na+ channel blockers tetrodotoxin and lidocaine; (5) irIL-1 beta release is significantly increased by noradrenalin; such increase is antagonized by verapamil and the beta-blocker propranolol, but not by the alpha-blocker phentolamine. The present evidence suggests that irIL-1 beta released by rat hypothalamic explants following KCl depolarization is neuronal in origin.
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