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Am J Physiol Gastrointest Liver Physiol (August 22, 2003). doi:10.1152/ajpgi.00289.2003
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Submitted on July 9, 2003
Accepted on August 19, 2003

Norepinephrine effects on identified neurons of the rat dorsal motor nucleus of the vagus

Isabel Martinez-Pena y Valenzuela1, Richard C. Rogers2, Gerlinda E. Hermann2, and R. Alberto Travagli3*

1 Department of Internal Medicine- Gastroenterology, University of Michigan, Ann Arbor, MI, USA
2 Laboratory of Autonomic Neuroscience, Pennington Biomedical Research Center, Baton Rouge, LA, USA
3 Department of Internal Medicine- Gastroenterology, University of Michigan, Ann Arbor, MI, USA; Department of Physiology, University of Michigan, Ann Arbor, MI, USA

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

The dorsal motor nucleus of the vagus (DMV) receives more noradrenergic terminals than any other medullary nucleus; few studies, however, have examined the effects of norepinephrine (NE) on DMV neurons. We used whole cell patch clamp recordings in thin slices to determine the effects of NE on DMV neurons identified according to their gastric projections, and immunohistochemical techniques were employed to examine the distribution of tyrosine hydroxylase immunoreactive (TH-IR) fibers within the DMV. Of the DMV neurons tested, 25% were unresponsive to NE perfusion, while the remaining 75% responded to NE in a concentration-dependent manner with either an excitation (49%), an inhibition (26%) or an inhibition followed by an excitation (4%). Antrum/pylorus- and corpus-projecting neurons responded to NE with a similar percentage of excitatory (49% and 59%, respectively) and inhibitory (20% for both groups) responses. A lower percentage of excitatory (37%) and a higher percentage of inhibitory (36%) responses were, however, observed in fundus-projecting neurons. In all groups, pretreatment with prazosin (100nM) or phenylephrine (10µM) antagonized or mimicked the NE-induced excitation, respectively. Conversely, pretreatment with yohimbine (10 µM) or UK-14304 (1µM) antagonized or mimicked the NE-induced inhibition, respectively. These data suggest that NE depolarization is mediated by {alpha}1-adrenoceptors, while NE hyperpolarization is mediated by {alpha}2-adrenoceptors. In sixteen neurons depolarized by NE, the amplitude of the action potential afterhyperpolarization (AHP) and its kinetics of decay ({tau}) were reduced by 13±0.7% and by 20±8% respectively (P<0.05 vs. control). No differences were found on the amplitude and {tau} of the AHP in neurons hyperpolarized by NE. Areas of significant difference in the TH-IR fiber density were observed within the mediolateral extent of the DMV; however, the mediolateral distribution of cells showing the different responses to NE did not show a pattern of localization.




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