Proceedings of The Physiological Society

University of Manchester (2010) Proc Physiol Soc 19, PC273

Poster Communications

Peripheral serotonin specific reuptake inhibitors (SSRI) acutely blunt sweet taste, and enhance salt taste in healthy humans.

T. Browning1, E. Bryant1, R. Jackson1, A. Smith1, J. K. Melichar1, L. F. Donaldson1

1. Physiology and Pharmacology, University of Bristol, Bristol, United Kingdom.


Serotonin has been hypothesised to act as a neurotransmitter both within the taste bud and between taste cells and gustatory afferents (1). We previously reported that lingually applied serotonin reuptake inhibitor (SSRI) acutely blunts bitter taste (2). SSRI are themselves bitter tasting compounds however, and therefore this observation may reflect bitter adaptation rather than an effect of serotoninergic modulation on taste perception per se. Sweet (n=10, 4 male, 6 female) and salt (n=30, 15 male, 15 female) recognition thresholds were determined in healthy volunteers (age range 18-51) at the tip of the tongue at each of four experimental sessions. Different concentrations of sweet (sucrose) and salt (NaCl) solutions (100mM to 1mM, ¼ log concentration steps) were presented to each subject in a pseudorandom order, using cotton buds soaked in each solution. Each taste concentration was presented a minimum of 5 times before and 10 minutes after drug (2mg.ml-1, 1 mg.ml-1, 0.5 mg.ml-1 paroxetine, diluted from 2mg.ml-1 in placebo) or placebo (proprietary glycerol based mixture) applied directly to the tongue in the area of testing. Drugs were all citrus flavoured. Psychophysical taste functions were constructed for each taste and drug to calculate mean taste thresholds. Data shown are mean ±95% confidence intervals. All protocols were approved by the Faculty of Medical and Veterinary Sciences Ethics committee, University of Bristol. Lingually applied SSRI exerted dose dependent effects on both salt and sweet taste thresholds. Lingual paroxetine (2mg.ml-1) resulted in a significant increase in sweet recognition threshold (before drug, 20mM (18 to 22mM); after placebo, 23mM (15 to 36mM); after paroxetine , 27mM (23 to 32mM), p<0.01, F test, 17% increase) after 10 minutes. In contrast in the same subjects, 2mg.ml-1 lingual paroxetine decreased salt recognition threshold (before drug, 11mM (9 to 14mM); after placebo, 9.5mM (7 to 13mM); after paroxetine 5mM (3 to 8mM), p<0.05, F test, 47% decrease). These data, together with the observation that bitter taste thresholds are also blunted by local SSRI, suggest that the effects of SSRI on taste thresholds are a drug effect, rather than bitter adaptation. These data show that acute inhibition of 5-HT reuptake at the taste bud blunts sweet taste (increases threshold) and enhances salt taste (decreases threshold). A model for 5-HT signaling in the taste bud will be presented.

Where applicable, experiments conform with Society ethical requirements