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According to a research group which is led by Professor Makoto Tominaga and Research Assistant Professor Hitoshi Inada (National Institute for Physiological Sciences, Okazaki, Japan) has found out that sour taste receptor, PKD1L3-PKD2L1 channel complex, might be generated by acid stimulus but opened way only after the eradication of acid stimulus. The researchers call it as a new type of response as ¡°off-response¡± of our sour taste receptor.
They examined the PKD1L3-PKD2L1 channel movement which is stimulated by acid stimulus with calcium imaging technique and electrophysiology. The cells conveying PKD1L3-PKD2L1 channels illustrated a considerable increase in intracellular Ca2+ but not while the acid stimulation was being washed out. The off-response property was verified by the complete cell patch-clamp configuration.
Prof Tominaga and Dr. Inada said ¡°The PKD1L3-PKD2L1 channels exist on the taste bud in the side and the inner part of tongue, where the salivary glands are close. Acidic things such as spoiled foods and harmful solutions are supposed to be dangerous to human body so that they should be quickly removed by saliva. The off-response of PKD1L3-PKD2L1 channels, we found here, helps human to keep sour taste sensation even after acid stimulus has been washed out.¡± The findings of the report have been published on June 6, 2008 in an international journal, EMBO.




 


 

 

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Sour taste finds closure in a potassium channel
Rosemary C. Challis and Minghong Ma
PNAS January 12, 2016 113 (2) 246-247; published ahead of print December 30, 2015 https://doi.org/10.1073/pnas.1523319113

Taste cells in taste buds of the mammalian tongue and oral cavity can detect five basic modalities: sweet, bitter, umami, salty, and sour. Each taste cell expresses distinct molecular sensors, such as G protein-coupled receptors or ion channels, which detect tastants (i.e., chemical stimuli that elicit taste sensation) and initiate an intracellular response that culminates in membrane depolarization and/or action potentials (APs) causing transmitter release. The race to solve the molecular identity of taste receptors more than 20 y ago sparked a revolution in gustatory physiology. The transduction components for sweet, bitter, umami, and salty taste have since been documented (1, 2), but sour taste remains poorly understood. The sour taste machinery has begun to emerge in recent years, but the intracellular response underlying sour taste detection is not known. In PNAS, Ye et al. (3) report a potassium (K+) channel as a key component of sour taste transduction, which fills a significant gap in the field.

Many ion channels have been proposed to mediate sour taste transduction, including a transient receptor potential (TRP) channel PKD2L1 and its partner PKD1L3 (4⇓⇓⇓⇓⇓⇓–11). Involvement of PKD family members in sour detection is supported by the fact that selective ablation of PKD2L1 cells nearly eliminates acid-induced responses in mouse gustatory nerve recordings (12). However, the functions of PKD2L1/PKD1L3 channels in sour taste remain enigmatic, given that genetic ablation of these channels has only a modest impact on acid-induced responses (13, 14). Nevertheless, PKD2L1 is a valuable molecular marker for sour cells (or type III taste cells), and its characterization has paved the way for the discovery of a Zn2+-sensitive proton conductance in PDK2L1 cells, which is believed to be the initial sour taste transduction event (15).

The current consensus in the field is that upon acid stimulation (Fig. 1A), protons are shuttled into the cell via a proton channel, which ultimately leads to cell depolarization and the firing of APs. How the proton conductance mediates cell depolarization remains unknown, but previous studies have hinted at a potential role of cytosolic acidification in sour taste transduction. This hypothesis stems from the observation that weak acids, which can diffuse across the lipid bilayer, evoke stronger responses in the gustatory nerve compared with strong acids (at the same pH), which cannot diffuse across the cell membrane (16, 17) (Fig. 1A). Moreover, the proton conductance measured in sour taste cells in response to extracellular acid is likely insufficient to elicit APs on its own (18). Together, these data point to intracellular acidification as a second component of sour taste transduction. Until now, this hypothesis has not been directly tested.

 
Potential contribution of the KIR2.1 channel in sour and nonsour taste cells. (A) In sour (PKD2L1) taste cells, weak acid causes stronger AP firing (Upper) than strong acid (Lower) at the same pH, presumably by intracellular acidification. (B, Upper) In nonsour (TRPM5) taste cells, weak acid stimulation does not cause AP firing, likely due to the large KIR2.1 current. (B, Lower) When the KIR2.1 current is mostly blocked, weak acid stimulation can cause AP firing.

Here, Ye et al. (3) tested whether intracellular acidification mediates the sour taste response. To prevent contributions from endogenous proton conductance, Zn2+ was used to block the proton channel in all experiments. By recording weak acid-induced responses from genetically labeled sour taste cells (PKD2L1-YFP) and nonsour taste cells (TRPM5 cells for sweet, umami, or bitter sensing), the authors found that APs are evoked in PKD2L1 cells but not in TRPM5 cells, supporting that only sour taste cells are sensitive to cytosolic acidification. How then does intracellular acidification generate depolarization and APs in sour taste cells? Cell depolarization may be caused by either inward Na+ or Ca2+ current or inhibition of outward K+ current. Ye et al. (3) explored each of these possibilities, including the potential role of PKD2L1, and discovered that cytosolic acidification has an exclusive impact on resting K+ currents in PKD2L1 cells by blocking K+ conductance. Although pH-sensitive K+ channels are known to be expressed in the taste epithelium (9, 11), this demonstration is the first, to our knowledge, that cytosolic acidification excites sour taste cells by directly blocking the resting K+ current.

To identify the acid-sensitive resting K+ current, Ye et al. (3) used transcriptome analysis and pharmacological profiling, which, together, implicate KIR2.1 as the source of the pH-sensitive K+ conductance (Fig. 1A). The authors then went on to demonstrate that heterologous expression of KIR2.1 confers sensitivity to acids, and that tissue-specific ablation of KIR2.1 in PKD2L1 cells significantly reduces the magnitude of the resting K+ current. These results strongly suggest that KIR2.1 functions to amplify the sensory response to sour taste stimuli.

Surprisingly, KIR2.1 is not only expressed in sour taste cells but also in TRPM5 cells. Why does cytosolic acidification evoke APs in sour taste cells but not in nonsour taste cells, even though both cell types express KIR2.1? To answer this question, Ye et al. (3) compared the magnitude of the resting K+ current in PKD2L1 and TRPM5 cells. Intriguingly, TRPM5 cells exhibit much larger K+ currents compared with PKD2L1 cells, presumably due to a greater density of KIR2.1 channels on the cell surface (Fig. 1B). This larger outward K+ current renders nonsour taste cells insensitive to intracellular acidification because more KIR2.1 channels would need to be closed to depolarize the cell and elicit a response. Surely enough, the authors show that when the magnitude of the resting K+ currents is reduced in nonsour cells, APs are fired upon weak acid stimulation (Fig. 1B). These data indicate that the small magnitude of the K+ current, rather than specific expression of KIR2.1 itself, facilitates the sour taste response. Furthermore, because PKD2L1 cells, but not TRPM5 cells, display a Zn2+-sensitive proton conductance in response to changes in cytosolic pH, the authors conclude that proton entry blocks the KIR2.1-mediated resting K+ current exclusively in sour taste cells. Together, Ye et al. (3) propose a mechanism for sour taste signaling in which KIR2.1 functions downstream of proton influx to amplify the sensory response. This mechanism resembles G protein-mediated olfactory transduction in which a Ca2+-activated Cl− current amplifies the initial depolarization caused by opening of the cyclic-nucleotide gated channel (19).

This study offers a plausible explanation to the long-sought mystery of why weak acids taste sourer than strong acids (at the same pH): by cytosolic acidification and downstream inhibition of KIR2.1. Future studies are needed to tease out the potential contributions of other ion channels reported in sour taste cells and achieve a comprehensive understanding of how these channels orchestrate sour detection under various conditions. This work also has broad implications for the function of KIR2.1, which is ubiquitously expressed in many organs throughout the body, including the brain, heart, kidney, and muscles (20). Understanding how diverse cell types might detect and perceive acid stimuli could inform the role of acid-sensitive receptor cells outside of the taste system, further expanding our knowledge of the mammalian chemosensory repertoire.