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Received October 7, 2004
Revised October 29, 2004
Accepted after revision November 5, 2004
1 Pennington Biomedical Research Center
* To whom correspondence should be addressed. E-mail: rogersrc{at}pbrc.edu.
Summary The nucleus of the solitary tract (NST) processes substantial visceral afferent input and sends divergent projections to a wide array of CNS targets. The NST is essential to the maintenance of behavioral and autonomic homeostasis and is the source, as well as the recipient, of considerable noradrenergic (NE) projections. The significance of NE projections from the NST to other CNS regions has long been appreciated, but the nature of NE action on NST neurons themselves, especially on the alpha -1 receptor subtype, is controversial. We used a combination of methodologies to establish, systematically, the effects and cellular basis of action of the alpha-1 agonist, phenylephrine (PHE), to control NST neurons responsible for vago-vagal reflex regulation of the stomach. Immunocytochemical and retrograde tracing studies verified that the area postrema, A2, A5, ventrolateral medulla, and locus coeruleus regions are sources of catecholaminergic input to the NST. In vivo electrophysiological recordings showed that PHE activates physiologically identified, second-order gastric sensory NST neurons. In vivo microinjection of PHE onto NST neurons caused a significant reduction in gastric tone. Finally, in vitro calcium imaging studies revealed that PHE caused dramatic cytosolic calcium oscillations in NST neurons. These oscillations are probably the result of an interplay between agonist-induced and inositol triphosphate (IP3)-mediated intracellular calcium release and calcium-ATPase control of intracellular calcium storage pumps. The oscillations persisted even in perfusions of zero calcium-EGTA Krebs suggesting that the calcium oscillation is mediated principally by intracellular calcium release-reuptake mechanisms. Cyclical activation of the NST may function to increase the responsiveness of these neurons to incoming afferent input (i.e., elevate the "gain"). An increase in gain of afferent input may cause an amplification of the response part of the reflex and help explain the powerful effects that alpha-1 agonists have in suppressing gastric motility and producing anorexia.
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