Cellular responses of NG108-15 and SK-N-MC lines to sweet and bitter tastants as measured by extracellular acidification rates

Citation
S. Khare et al., Cellular responses of NG108-15 and SK-N-MC lines to sweet and bitter tastants as measured by extracellular acidification rates, J NEUROSC R, 63(1), 2001, pp. 64-71
Citations number
20
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE RESEARCH
ISSN journal
03604012 → ACNP
Volume
63
Issue
1
Year of publication
2001
Pages
64 - 71
Database
ISI
SICI code
0360-4012(20010101)63:1<64:CRONAS>2.0.ZU;2-Z
Abstract
The Cytosensor microphysiometer device (Molecular Devices, Sunnyvale, CA) i s capable of detecting small changes in cellular metabolism in response to specific bioactive ligands by measuring the extracellular acidification rat e (ECAR), By measuring the ECAR we were able to detect responses of tissue culture cell lines to a variety of sweet- and bitter-tasting compounds. We examined in detail the responses of the NG108-15 (mouse neuroblastoma x rat glioma hybrid) and SK-N-MC (human neuroepithelioma) cell lines. We determi ned that NG108-15 cells were consistently very responsive to several potent sweeteners and bitter compounds, such as sodium saccharin, guanidino- swee teners, denatonium benzoate, quinine, and ranitidine. These compounds could evoke changes in cellular metabolism (measured as ECAR) that were rapid in onset, saturable with respect to ligand concentration, and sensitive to se veral inhibitors of G-protein-coupled receptor signaling pathways. In sharp contrast, the neuroepithelioma SK-N-MC did not respond to any of the sweet or bitter compounds. Rapid changes in ECAR were easily detectable in both cell lines with the calcium ionophore A23187. Bradykinin elicited changes i n the ECAR only in the NG108-15 cell line, which is known to express the B2 receptor. The changes in ECAR of the NG108-15 cell line in response to swe et and bitter taste compounds suggest these cells may expresses a receptor( s) specific for small sapid molecules. (C) 2001 Wiley-Liss, Inc.