RT Journal Article
SR Electronic
T1 Antagonism of the gerbil's sucrose taste response by p-nitrophenyl alpha-D-glucopyranoside and chloramphenicol
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 2611
OP 2615
DO 10.1523/JNEUROSCI.06-09-02611.1986
VO 6
IS 9
A1 Vlahopoulos, V
A1 Jakinovich, W
YR 1986
UL http://www.jneurosci.org/content/6/9/2611.abstract
AB We have discovered that the gerbil's chorda tympani nerve response to sucrose is suppressed by p-nitrophenyl alpha-D-glucopyranoside (PNP- Glu) and chloramphenicol (CAP). Mixture experiments of PNP-Glu and CAP with sodium chloride, potassium chloride, hydrochloric acid, and sucrose gave rise to the following observations: Neither PNP-Glu nor CAP alone stimulates the gerbil's taste nerve; while the sucrose response is suppressed by these inhibitors, taste responses produced by sodium chloride, potassium chloride, and hydrochloric acid are unaffected by the presence of PNP-Glu or CAP; the antagonisms of PNP- Glu and CAP were surmounted by a high concentration of sucrose; CAP is a more potent antagonist (IC50 = 0.0013 M) than PNP-Glu (IC50 = 0.022 M), and both are more potent than methyl 4,6-dichloro-4,6-dideoxy-alpha- D-galactopyranoside (IC50 = 0.048 M); and sucrose antagonism occurs only when PNP-Glu and CAP are mixed with sucrose. It is short-lived and ceases when the mixtures are rinsed from the gerbil's tongue. Structure- activity studies provided the following information: The alpha anomer of PNP-Glu is a more potent inhibitor than its beta anomer; among the PNP-Glu derivatives tested (p-aminophenyl, p-nitrophenyl, and phenyl) only p-nitrophenyl inhibited; among the nitrophenyl galactosides, the para derivative was more potent than the ortho or meta; and p- nitrophenyl alpha-D-mannopyranoside and p-nitrophenyl alpha-D- galactoside are slightly more potent than PNP-Glu. On the basis of concentration experiments, we believe that the inhibitory mechanisms of PNP-Glu and CAP are different, which suggests the existence of at least 2 sucrose receptor sites.