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Immunocytes modulate ganglionic nitric oxide release which later affects their activity level.
George B Stefano1, Kirk Mantione, Dolisha Jones
1Neuroscience Research Institute, State University of New York College at Old Westbury, Old Westbury, NY 11568-0210, USA. gstefano@sunynri.org
Neuro Endocrinology Letters
|May 26, 2004
Summary
Activated immunocytes stimulate nitric oxide (NO) release from pedal ganglia. This NO release, inhibited by L-NAME, down-regulates immunocyte activity, revealing a novel neuro-immune signaling pathway.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Pedal ganglia release nitric oxide (NO) in vitro.
- Immunocytes can modulate NO release from ganglia.
- Interleukin-1 beta activates immunocytes.
Purpose of the Study:
- To investigate the interaction between pedal ganglia and immunocytes.
- To determine the role of nitric oxide in this interaction.
- To explore the signaling pathway involved in immunocyte activation and regulation.
Main Methods:
- Organotypic culture of pedal ganglia.
- Incubation of ganglia with activated and non-activated immunocytes.
- Measurement of nitric oxide release.
- Inhibition of nitric oxide synthase with L-NAME.
- Assessment of immunocyte morphology and activity levels.
Main Results:
- Activated immunocytes significantly increase NO release from pedal ganglia.
- L-NAME, a nitric oxide synthase inhibitor, blocks this NO release.
- Ganglionic NO release down-regulates the activity of activated immunocytes.
- Immunocyte activation is confirmed by changes in cell morphology (form factors).
Conclusions:
- Pedal ganglia release nitric oxide in response to activated immunocytes.
- Nitric oxide acts as a signaling molecule to modulate immunocyte activity.
- This study elucidates a novel neuro-immune communication pathway involving NO.