Submitted on October 26, 2006
Accepted on February 13, 2007
Gastric vagal efferent inhibition evoked by intravenous CRF is unrelated to simultaneously recorded vagal afferent activity in urethane-anesthetized rats
David W. Adelson1*, Hovsep P. Kosoyan1, Yuhua Wang2, Justin Z. Steinberg2, and Yvette Tache3
1 CURE: Digestive Diseases Research Center and Center for Neurovisceral Sciences & Women's Health, Division of Digestive Diseases, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, California, United States; West Los Angeles Veterans Affairs Medical Center, VA Greater Los Angeles Healthcare System, Los Angeles, California, United States
2 CURE: Digestive Diseases Research Center and Center for Neurovisceral Sciences & Women's Health, Division of Digestive Diseases, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, California, United States
3 United States; CURE: Digestive Diseases Research Center and Center for Neurovisceral Sciences & Women's Health, Division of Digestive Diseases, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, California, United States; West Los Angeles Veterans Affairs Medical Center, VA Greater Los Angeles Healthcare System, Los Angeles, California, United States
* To whom correspondence should be addressed. E-mail: dadelson{at}ucla.edu.
Corticotropin-releasing factor (CRF) injected peripherally or released in response to stressful challenges to the organism, reduces gastric tone and contractility, in part via vagal pathways. However, information on the changes in gastric vagal impulse activity evoked by peripheral CRF administration is entirely lacking. Using a novel 'dual recording' method in urethane-anesthetized rats, vagal efferent (VE) and afferent (VA) impulse activities were recorded simultaneously from separate, fine bundles dissected from the ventral gastric vagus nerve branch innervating the glandular stomach. Activity records for 38 VA single units (SUs) and 33 VE SUs were sorted from multi-unit records obtained from 13 preparations. Saline (iv) had no effect on multi-unit VE activity, while CRF (1 µg/kg, iv) immediately inhibited VE activity, reaching a nadir of 54 ± 8.0% of pre-injection levels at 3.0 min post injection. CRF (1 µg/kg, iv) inhibited 25/33 (75.8%) VE SUs and excited 3/33 (9.1%) VE SUs. In contrast to potent effects on VE activity, iv CRF did not alter multi-unit VA activity. Single-unit analysis, however, revealed 5/38 (13.1%) VA SUs excited by iv CRF at widely varying latencies (suggesting an indirect mode of action), and one inhibited VA SU. VA SUs excited following iv CRF did not respond during gastric distention and vice-versa. These experiments are the first employing simultaneous recording of gastric VA and VE units. The data demonstrate a predominantly inhibitory influence of iv CRF on VE outflow to the hindstomach, not driven by gastric vago-vagal reflex activity.
