A research group led by Assistant Professor Kengo Horie and Professor Ryusuke Yoshida from the Department of Oral Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences at Okayama University has revealed that mice with taste cell-specific deletion of synapse-related genes cannot maintain sour taste receptor cells and show reduced responses only to sour taste. Since sweet, umami, salty, and bitter tastes were unaffected, the findings revealed that multiple neural mechanisms are involved in taste information processing. The study was published in The Journal of Physiology.
A) Taste tissue of wild-type mice and taste cell synapse deficiency mice (SNAP-cKO). SNAP-cKO mice show a reduction in acid taste cells.
B) Taste nerve responses to various taste stimuli in wild-type mice (red) and SNAP-cKO mice (blue).
In SNAP-cKO mice, responses to sour stimuli (HCl, citric acid, acetic acid, lactic acid, tartaric acid) were reduced compared to wild-type mice, but responses to sweet, salty, bitter, and umami stimuli showed no significant differences.
Provided by Okayama University
Taste cells that detect the five basic tastes (sweet, umami, salty, bitter, and sour) are found on the tongue, soft palate, and pharynx, where they detect taste substances (chemical compounds) in the mouth and transmit taste information to nerves. Previous research had revealed that the structure of chemical synapses that ordinarily serve as sites for interneural information exchange (the mechanism by which nerve cells transmit information to other cells through the release of neurotransmitters) is found only in some taste cells. However, it remained unclear how chemical synapses in taste cells actually contribute to taste information transmission.
Although various proteins are involved in neurotransmitter release at chemical synapses, the researchers created mice with taste cell-specific deletion of SNAP25 (a protein involved in neurotransmitter release from presynaptic cells), which is known to be expressed in taste cells, and examined mouse responses to various taste stimuli. In taste cell SNAP25-deficient mice, neural responses to sour stimuli such as citric acid, acetic acid, and HCl were eliminated, but neural responses to sucrose (sweet), sodium glutamate (umami), NaCl (salty), and quinine (bitter) were unchanged compared with normal mice. When behavioral responses to various taste solutions were examined, taste cell SNAP25-deficient mice showed weakened avoidance responses to sour taste. Furthermore, examination of taste bud tissue in taste cell SNAP25-deficient mice revealed a decrease in the number of sour taste receptor cells, indicating that this was due to impaired maintenance of sour taste receptor cells.
Taste disorders include conditions where sensitivity to specific tastes becomes impaired (dissociative taste disorders). The current results suggest that abnormalities in taste cell synapses may be involved as a cause of sour taste-specific taste disorders. Furthermore, the mice created in this study could potentially be developed into model mice for various neurological diseases such as Parkinson's disease.
Yoshida commented: "Among the five basic tastes (sweet, umami, salty, bitter, and sour), questions such as 'Why do only taste cells that detect sour taste utilize chemical synapses?' and 'What are the differences between these and the taste cells that detect other tastes?' still remain. I believe this research represents a landmark that demonstrates the fascinating nature of taste."
Journal Information
Publication: The Journal of Physiology
Title: Dual functions of SNAP25 in mouse taste buds
DOI: 10.1113/JP288683
This article has been translated by JST with permission from The Science News Ltd. (https://sci-news.co.jp/). Unauthorized reproduction of the article and photographs is prohibited.