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. Author manuscript; available in PMC: 2022 Dec 1.
Published in final edited form as: Auton Neurosci. 2021 Sep 11;236:102874. doi: 10.1016/j.autneu.2021.102874

Fig. 2.

Fig. 2.

Genetic Deletion or Pharmacological Block of P2X3 and P2X2/P2X3 channels eliminates taste responses and behaviors. A. Taste nerve (chorda tympani) recordings comparing responses in P2X2/P2X3 double KO mice (Right column) with WT controls (Left column) on the same mixed background for selected taste substance (Sucrose = sweet; QHCl, Quinine HCl = bitter; Citric Acid = sour). Responses in the KO animals are absent although the KO nerves still respond to temperature and touch. B. Graphs comparing taste preference behavior in P2X2/P2X3 double KO and WT mice in aa 2 bottle preference test. The ordinate shows the ratio of tastant consumed compared to water. WT animals (black) strongly prefer the artificial sweetener and avoid the bitter compound, denatonium. In contrast, KO animals (red) show neither preference nor avoidance to the respective tastants. C. Nerve recordings in WT animals injected with the antagonist AF-353 which inhibits all P2X3 containing receptors. Top trace (black) shows responses to all tastants; the drug-treated animal shows virtually no taste responses (red) to any tastant. NH4Cl = ammonium chloride; Cit. Acid = citric acid, MSG = monosodium glutamate. D. Tastant-evoked behavior in WT mice treated either with vehicle or with AF-353. Vehicle-treated mice show increasing preference for the artificial sweetener whereas the AF-353-treated animals show no response to this sweetener. Panels A & B adapted from (Finger et al. 2005). Panels C & D adapted from (Vandenbeuch et al. 2015).