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Intracisternal sauvagine is more potent than corticotropin-releasing factor to decrease gastric vagal efferent
H P Kosoyan1, J Y Wei, Y Taché
1CURE, Digestive Diseases Research Center, West Los Angeles Veterans Administration Medical Center, California 90073, USA. hkosoyan@ucla.edu
Peptides
|September 7, 1999
Summary
Corticotropin-releasing factor (CRF) and sauvagine inhibit gastric vagal efferent multiunit discharge (GVED) in rats. Endogenous CRF also plays a role in regulating GVED.
Area of Science:
- Neuroendocrinology
- Gastrointestinal Physiology
- Autonomic Nervous System Function
Background:
- The role of corticotropin-releasing factor (CRF) in regulating gastrointestinal functions is increasingly recognized.
- CRF and related peptides like sauvagine are known to influence autonomic pathways.
- Gastric vagal efferent activity is a key regulator of gastric function.
Purpose of the Study:
- To investigate the effect of intracisternal administration of CRF and sauvagine on gastric vagal efferent multiunit discharge (GVED) in rats.
- To determine the potency of sauvagine relative to CRF in modulating GVED.
- To examine the role of endogenous CRF in maintaining basal GVED.
Main Methods:
- Rats anesthetized with urethane underwent intracisternal injections of CRF, sauvagine, or vehicle.
- Gastric vagal efferent multiunit discharge (GVED) was recorded before and after injections.
- A specific CRF antagonist was used to block CRF-induced effects and assess endogenous CRF tone.
Main Results:
- Both CRF and sauvagine dose-dependently decreased GVED.
- Sauvagine was found to be more potent than CRF in inhibiting GVED.
- CRF antagonist administration increased GVED and blocked CRF-induced inhibition, suggesting endogenous CRF exerts an inhibitory tone.
Conclusions:
- CRF and sauvagine inhibit GVED via CRF receptors.
- Sauvagine exhibits greater potency than CRF in this inhibitory action.
- Endogenous CRF contributes to the regulation of basal GVED in anesthetized rats.