Imagine what your childhood would have been like if you could never experience the tantalizing taste of a WarHead or the painfully-pleasing sensation of biting into a sour lemon? What if you suddenly couldn’t appreciate the sour beer filing your mug on a warm spring night? While most of our neurons are contained within our brain, life would certainly not be the same without the complete set of cells comprising our nervous system.
Dr. Emily Liman researches the physiological basis of perceiving sensations such as pain and taste. Recently, Dr. Liman revealed that sour transduction is mediated by a proton current enriched on the apical surface of taste cells. Strong acids can activate this proton current, causing the cell to fire a burst of action potentials and generate an acid-evoked inward current. Previously, the PKD2L1/PKD1L3 heterodimer was identified as a marker for sour taste cells, however the function of this channel is not necessary for perceiving sour taste. In the current study, Dr. Liman used transgenic mice, calcium imaging and electrophysiological recordings to identify the elusive mechanism of sour transduction.
Do you remember stuffing your mouth with a fistful of sour patch kids or gummy worms? A variety of acids were responsible for the delicious yet tarty taste you experienced. Similarly, Dr. Liman demonstrated that stimulating PKD2L1-expressing cells with hydrochloric acid (HCl; pH 5) or acetic acid (HOAc; pH 5) induced a rapidly inactivating inward current in those cells (Fig. 2A, B). This cellular response was even present in sour taste cells lacking functional PKD2L1/PKD1L3 channels (Fig. 2C), supporting that an alternative mechanism contributes to sour transduction. Since this acid-response must be mediated by some molecular mechanism, a variety of pharmacological agents were used to alter the concentration of Na+, Ca2+ or Cl–, testing the possibility that a cation or anion mediates the cell’s response to acid. However, these manipulations revealed that a sour taste cell’s response to an acid is not mediated by an ionic conductance (Fig. 2C). Instead, H+ is the likely charge carrier allowing a sour taste cell to respond to extracellular acidification.
Interestingly, pharmacological agents such as Bafilomycin, Cd2+, Desipramine and Amiloride, which block proton currents, had no effect on reducing the acid-evoked inward current. Only Zn2+, which is known to block many channels including the proton channel, Hv1, could inhibit the acid-response in sour taste cells (Fig. 3D).
Additionally, Dr. Liman used UV uncaging of NPE-caged protons and Ca2+ microfluorimetry to measure how a cell might respond to extracellular acidification. In this manner, a proton current was simulated by uncaging protons at the apical surface of the sour taste cell. Calcium imaging showed that sour taste cells responded to the uncaged protons with a burst of action potentials, a large inward current, and an elevation of intracellular Ca2+ (Fig. 5B).
While the specific mechanism underlying the proton current remains a mystery (a proton channel or transporter are the likely candidates), I’ll personally sleep better at night knowing that I’ll wake up with my sour taste cells intact and ready to enjoy a warm cup of tea infused with freshly cut lemon.
Come and hear Dr. Emily Liman’s talk — Taste and the single cell: Uncovering mechanisms of sour transduction, Tuesday, March, 17th at 4pm in the Center for Neural Circuits and Behavior Marilyn C. Farquhar Conference Room.
Bankole Aladesuyi is a first-year Neurosciences student currently rotating with Dr. Xin Jin. When not reminiscing about a childhood spent eating candy for lunch, he enjoys playing soccer, making music and reading science fiction.
Chang, R. B., Waters, H., & Liman, E. R. (2010). A proton current drives action potentials in genetically identified sour taste cells. Proceedings of the National Academy of Sciences, 107(51), 22320-22325.