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The Journal of Neurophysiology Vol. 86 No. 5 November 2001, pp. 2638-2641
Copyright ©2001 by the American Physiological Society
RAPID COMMUNICATION
1Department of Physiology, Virginia Commonwealth University, Richmond 23298-0551; 2McGuire Veterans Affairs Medical Center, Richmond, Virginia 23249; and 3GlaxoSmithKline, Parsippany, New Jersey 07054
DeSimone, John A.,
Vijay Lyall,
Gerard L. Heck,
Tam-Hao T. Phan,
Rammy I. Alam,
George M. Feldman, and
R. Michael Buch.
A Novel Pharmacological Probe Links the Amiloride-Insensitive
NaCl, KCl, and NH4Cl Chorda Tympani Taste Responses. J. Neurophysiol. 86: 2638-2641, 2001. Chorda tympani taste nerve responses to NaCl can be dissected
pharmacologically into amiloride-sensitive and -insensitive components.
It is now established that the amiloride-sensitive, epithelial sodium
channel acts as a sodium-specific ion detector in taste receptor cells
(TRCs). Much less is known regarding the cellular origin of the
amiloride-insensitive component, but its anion dependence indicates an
important role for paracellular shunts in the determination of its
magnitude. However, this has not precluded the possibility that
undetected apical membrane ion pathways in TRCs may also contribute to
its origin. Progress toward making such a determination has suffered
from lack of a pharmacological probe for an apical
amiloride-insensitive taste pathway. We present data here showing that,
depending on the concentration used, cetylpyridinium chloride (CPC) can
either enhance or inhibit the amiloride-insensitive response to NaCl.
The CPC concentration giving maximal enhancement was 250 µM. At 2 mM,
CPC inhibited the entire amiloride-insensitive part of the NaCl
response. The NaCl response is, therefore, composed entirely of
amiloride- and CPC-sensitive components. The magnitude of the maximally
enhanced CPC-sensitive component varied with the NaCl concentration and was half-maximal at [NaCl] = 62 ± 11 (SE) mM. This was
significantly less than the corresponding parameter for the
amiloride-sensitive component (268 ± 71 mM). CPC had similiar
effects on KCl and NH4Cl responses except that in
these cases, after inhibition with 2 mM CPC, a significant
CPC-insensitive response remained. CPC (2 mM) inhibited intracellular
acidification of TRCs due to apically presented
NH4Cl, suggesting that CPC acts on an apical
membrane nonselective cation pathway.
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