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Received April 5, 2002
Accepted after revision June 26, 2002
1 College of Dentistry, Ohio State University, 305 West 12th Avenue, P.O. Box 182357, Columbus, OH 43218-2357, USA
2 Department of Oral Biology, College of Dentistry, Ohio State University, 305 West 12th Avenue, Columbus, OH 43210, USA
3 Preclinical Toxicology Infectious Disease/Safety Pharmacology, Pharmacia Corporation, 7270-300-130, 301 Henrietta Street, Kalamazoo, MI 49007, USA
* To whom correspondence should be addressed. E-mail: herness.1{at}osu.edu.
In taste buds, synaptic transmission is traditionally thought to occur from taste receptor cells to the afferent nerve. This communication reports the novel observation that taste receptor cells respond to adrenergic stimulation. Noradrenaline application inhibited outward potassium currents in a dose-dependent manner. This inhibition was mimicked by the ß agonist isoproterenol and blocked by the ß antagonist propranolol. The
agonists clonidine and phenylephrine both inhibited the potassium currents and elevated intracellular calcium levels. Inwardly rectifying potassium currents were unaffected by adrenergic stimulation. Experiments using the RT-PCR technique demonstrate that lingual epithelium expresses multiple
(
1a,
1b,
1c,
1d,
2a,
2b,
2c) and ß (ß1, ß2) subtypes of adrenergic receptors, and immunocytochemistry localized noradrenaline to a subset of taste receptor cells. Collectively, these data imply strongly that adrenergic transmission within the taste bud may play a paracrine role in taste physiology.
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