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This Article Full Text Full Text (PDF) All Versions of this Article: 97/4/3004    most recent 01143.2006v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Adelson, D. W. Articles by Taché, Y. Search for Related Content PubMed PubMed Citation Articles by Adelson, D. W. Articles by Taché, Y.

Gastric Vagal Efferent Inhibition Evoked by Intravenous CRF Is Unrelated to Simultaneously Recorded Vagal Afferent Activity in Urethane-Anesthetized Rats

Center for Ulcer Research and Education, Digestive Diseases Research Center and Center for Neurovisceral Sciences and Women's Health, Division of Digestive Diseases, David Geffen School of Medicine at the University of California, Los Angeles and Veterans Administration Greater Los Angeles Healthcare System–West Los Angeles Veterans Affairs Medical Center, Los Angeles, California

Submitted 26 October 2006; accepted in final form 13 February 2007

Corticotropin-releasing factor (CRF) injected peripherally or released in response to stressful challenges to the organism reduces gastric tone and contractility, in part by 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 multiunit records obtained from 13 preparations. Intravenous (iv) administration of saline had no effect on multiunit VE activity, whereas CRF (1 µg/kg, iv) immediately inhibited VE activity, reaching a nadir of 54 ± 8.0% of preinjection levels at 3.0 min postinjection. CRF (1 µg/kg, iv) inhibited 25/33 (75.8%) VE SUs and excited three of 33 (9.1%) VE SUs. In contrast to potent effects on VE activity, iv CRF did not alter multiunit VA activity. Single-unit analysis, however, revealed five of 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 after iv CRF did not respond during gastric distention and vice versa. These experiments are the first to use 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 vagovagal reflex activity.