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Am J Physiol Regul Integr Comp Physiol 290: R1151-R1152, 2006; doi:10.1152/ajpregu.00584.2005
0363-6119/06 $8.00
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LETTERS TO THE EDITOR

APPETITE, OBESITY, DIGESTION, AND METABOLISM

Comments on "Hindbrain chemical mediators of reflex-induced inhibition of gastric tone produced by esophageal distension and intravenous nicotine"

Richard C. Rogers, Gerlinda E. Hermann and R. Alberto Travagli

Department of Neuroscience
Pennington Biomedical Research Center
Louisiana State University System
Baton Rouge, Louisiana

ABSTRACT

The purpose of this study was to activate a vagovagal reflex by using esophageal distension and nicotine and test whether hindbrain nitric oxide and norepinephrine are involved in this reflex function. We used double-labeling immunocytochemical methods to determine whether esophageal distension (and nicotine) activates c-Fos expression in nitrergic and noradrenergic neurons in the nucleus tractus solitarii (NTS). We also studied c-Fos expression in the dorsal motor nucleus of the vagus (DMV) neurons projecting to the periphery. Esophageal distension caused 19.7 ± 2.3% of the noradrenergic NTS neurons located 0.60 mm rostral to the calamus scriptorius (CS) to be activated but had little effect on c-Fos in DMV neurons. Intravenous administration of nicotine caused 19.7 ± 4.2% of the noradrenergic NTS neurons 0.90 mm rostral to CS to be activated and, as reported previously, had no effect on c-Fos expression in DMV neurons. To determine whether norepinephrine and nitric oxide were central mediators of esophageal distension-induced decrease in intragastric pressure (balloon recording), NG-nitro-L-arginine methyl ester microinjected into the NTS (n = 5), but not into the DMV, blocked the vagovagal reflex. Conversely, {alpha}2-adrenergic blockers microinjected into the DMV (n = 7), but not into the NTS, blocked the vagovagal reflex. These data, in combination with our earlier pharmacological microinjection data with nicotine, indicate that both esophageal distension and nicotine produce nitric oxide in the NTS, which then activates noradrenergic neurons that terminate on and inhibit DMV neurons.


 

REPLY

Manuel Ferreira, Jr., Niaz Sahibzada, Min Shi, Mark Niedringhaus, Matthew R. Wester, Allison R. Jones, Joseph G. Verbalis, and Richard A. Gillis

Departments of Pharmacology and Medicine (Endocrinology)
Georgetown University Medical Center
Washington, District of Columbia








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