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Am J Physiol Regul Integr Comp Physiol 285: R479-R489, 2003. First published April 24, 2003; doi:10.1152/ajpregu.00155.2003
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APPETITE, OBESITY AND METABOLISM

Noradrenergic neurons in the rat solitary nucleus participate in the esophageal-gastric relaxation reflex

R. C. Rogers,1 R. A. Travagli,2 and G. E. Hermann1

1Laboratory of Autonomic Neuroscience, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana 70808; and 2Departments of Internal Medicine-Gastroenterology and Physiology, University of Michigan, Ann Arbor, Michigan 48109

Submitted 26 February 2003 ; accepted in final form 22 April 2003

Activation of esophageal mechanosensors excites neurons in and near the central nucleus of the solitary tract (NSTc). In turn, NSTc neurons coordinate the relaxation of the stomach [i.e., the receptive relaxation reflex (RRR)] by modulating the output of vagal efferent neurons of the dorsal motor nucleus of the vagus (DMN). The NSTc area contains neurons with diverse neurochemical phenotypes, including a large population of catecholaminergic and nitrergic neurons. The aim of the present study was to determine whether either one of these prominent neuronal phenotypes was involved in the RRR. Immunohistochemical techniques revealed that repetitive esophageal distension caused 53% of tyrosine hydroxylase-immunoreactive (TH-ir) neurons to colocalize c-Fos in the NSTc. No nitric oxide synthase (NOS)-ir neurons in the NSTc colocalized c-Fos in either distension or control conditions. Local brain stem application (2 ng) of {alpha}-adrenoreceptor antagonists (i.e., {alpha}1-prazosin or {alpha}2-yohimbine) significantly reduced the magnitude of the esophageal distension-induced gastric relaxation to ~55% of control conditions. The combination of yohimbine and prazosin reduced the magnitude of the reflex to ~27% of control. In contrast, pretreatment with either the NOS-inhibitor NG-nitro-L-arginine methyl ester or the {beta}-adrenoceptor antagonist propranolol did not interfere with esophageal distension-induced gastric relaxation. Unilateral microinjections of the agonist norepinephrine (0.3 ng) directed at the DMN were sufficient to mimic the transient esophageal-gastric reflex. Our data suggest that noradrenergic, but not nitrergic, neurons of the NSTc play a prominent role in the modulation of the RRR through action on {alpha}1- and {alpha}2-adrenoreceptors. The finding that esophageal afferent stimulation alone is not sufficient to activate NOS-positive neurons in the NSTc suggests that these neurons may be strongly gated by other central nervous system inputs, perhaps related to the coordination of swallowing or emesis with respiration.

vagus; brain stem; c-Fos


Address for reprint requests and other correspondence: G. E. Hermann, Laboratory of Autonomic Neuroscience, Pennington Biomedical Research Center, 6400 Perkins Rd., Baton Rouge, LA 70808 (E-mail: hermange{at}pbrc.edu).




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