Neuroscience 2000 Abstract
| Presentation Number: | 433.8 |
|---|---|
| Abstract Title: | Effect of peripheral corticotropin-releasing factor (CRF), sauvagine and CRF<SUB>1</SUB> receptor antagonist (CP-154,526) on gastric vagal afferent discharge (GVAD) in rats. |
| Authors: |
Kosoyan, H. P.*1
; Taché, Y.1
1CURE/DDRC, VAGLAHS, and Department of Med & Brain Research Institute, UCLA, Los Angeles, CA |
| Primary Theme and Topics |
D. Neurotransmitters, Modulators, Transporters, and Receptors - 48. Peptides |
| Secondary Theme and Topics | E. Endocrine and Autonomic Regulation<br />- 64. Neuroendocrine regulation: other |
| Session: |
433. Peptides: physiology II Poster |
| Presentation Time: | Tuesday, November 7, 2000 11:00 AM-12:00 PM |
| Location: | Hall G-J |
| Keywords: | VAGUS, NERVE, PEPTIDE, CRF |
Our previous studies indicate that peripheral CRF dose-dependently activates gastric vagal afferent terminals that also respond to gastric distention and nonselective peptide antagonist of CRF (astressin) completely blocks CRF-induced activation of GVAD (SFN, 25, 387.12, 1999). Recent findings suggested, that the nonpeptide antagonist of CRF1 receptors (CP-154,526), administered systemically, antagonizes the stimulatory effects of exogenous CRF on plasma ACTH, locus coeruleus neuronal firing and startle response amplitude (Proc. Natl. Sci. USA, 93, 10477-10482, 1996). Aim: To assess the influence of CRF, sauvagine and selective, nonpeptide antagonist of CRF1 receptor (CP-154,526) injected intravenously (iv) on GVAD. Method: Male SD rats (280-320 g) were anesthetized with urethane and implanted with an intrajugular catheter for iv (0.1 ml) injection. A flexible, latex balloon was placed in the stomach via the incision for gastric distention (GD, 5 ml saline at 37° C). A strand of ventral gastric branch of the vagus was cut proximally to record afferent discharge. Nerve signals were sent to a window discriminator and counted on computer. Five minute maximum peak values from preinjection basal GVAD were calculated (Mean ± SEM). Results: In control experiments consecutive injections of vehicle (x2), CRF 126 pmol (x2) and sauvagine 126 pmol at 16th min, 34th min, 75th min, 122nd min and 176th min, and GD performed at 240th min significantly increased GVAD to 111.5±07%. 119.5±1.3%, 152.3±2.5%, 162.8±2.8% and 159.0±3.2% (F5,18=170.717, P<0.05), and 397±21.6% (F6,21=160.704), respectively. Saline did not cause significant change in basal GVAD (100.5±1.3%. In another group of animals (n=4) iv injections of vehicle and CP-154,526 (7mg/kg, pH=7.0), followed by saline had no significant effect on GVAD. CRF 126 pmol (x2) and sauvagine 126 pmol injected at 30th min, 70th min and 110th min, and GD performed at 154th min after the CP treatment, significantly increased GVAD to 138.8±23.4%, 149.8±18.7% and 156.8±19.2% (F5,18=3609, P<0.05), and 378.3±115.5% (F6,21=4.311), respectively. Conclusion: Peripheral CRF and sauvagine activates gastric vagal afferent terminals that also respond to gastric distention. CRF1 receptor antagonist (CP-154,526) did not significantly alter CRF-induced activation of vagal afferents. These data and our previous findings suggest that primarily CRF2 receptor subtype is involved in mediating the peripheral CRF-induced vagal afferent activity.
Supported by NIH grant DK30110.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2000 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2000. Online.
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