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Am J Physiol Regul Integr Comp Physiol (April 24, 2003). doi:10.1152/ajpregu.00155.2003
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Submitted on March 26, 2003
Accepted on April 22, 2003

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

Richard C Rogers1, R. Alberto Travagli2, and Gerlinda E Hermann1*

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

* To whom correspondence should be addressed. E-mail: hermange{at}pbrc.edu.

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 if 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 co-localize cFos in the NSTc. No nitric oxide synthase [NOS-ir] neurons in the NSTc co-localized cFos in either distension or control conditions. Local brainstem application [2ng] 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 approximately 55% of control conditions. The combination of yohimbine and prazosin reduced the magnitude of the reflex to approximately 27% of control. In contrast, pretreatment with either the NOS-inhibitor [L-NAME] or the beta-adrenoceptor antagonist [propranolol] did not interfere with esophageal-distension induced gastric relaxation. Unilateral microinjections of the agonist, norepinephrine [0.3ng], 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 suggest that these neurons may be strongly gated by other CNS inputs, perhaps related to the coordination of swallowing or emesis with respiration.




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