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Gustation, or the sense of taste, is intrinsically linked to the anatomical structures located on the tongue. This organ's surface, along with the entirety of the oral cavity, is adorned with stratified squamous epithelium. Evident on the tongue are elevated structures known as papillae (singular = papilla), which house the mechanisms for the transduction of gustatory stimuli. Four distinct types of papillae exist, each identified by their unique morphological attributes: the circumvallate,...
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The perception of a salty flavor is facilitated by sodium ions within the oral salivary fluid. Upon consumption of a salty substance, salt crystals disassemble, leading to the liberation of its constituents—Na+ and Cl- ions. These ions subsequently dissolve into the salivary fluid present in the oral cavity. The external environment of the gustatory cells experiences an elevation in Na+ concentration, thereby establishing a potent concentration gradient. This gradient propels the...
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Gustation is a chemical sense that, along with olfaction (smell), contributes to our perception of taste. It starts with the activation of receptors by chemical compounds (tastants) dissolved in the saliva. The saliva and filiform papillae on the tongue distribute the tastants and increase their exposure to the taste receptors.
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Conditioned taste aversion, also known as sauce béarnaise syndrome, is a phenomenon in which an individual develops an aversion to a certain food taste following a negative experience, typically illness. This form of aversion is a type of classical conditioning in which the taste of the food (conditioned stimulus, CS) is associated with the experience of illness (unconditioned stimulus, UCS).
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Related Experiment Video

Updated: Aug 7, 2025

Toxicity Study of Zinc Oxide Nanoparticles in Cell Culture and in Drosophila melanogaster
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Tongue-Brain-Transported ZnO Nanoparticles Induce Abnormal Taste Perception.

Aijie Chen1,2, Ruolan Wang3, Yiyuan Kang1

  • 1Stomatology Hospital, School of Stomatology, Southern Medical University, Guangzhou, 510515, China.

Advanced Healthcare Materials
|March 12, 2023
PubMed
Summary
This summary is machine-generated.

Zinc oxide nanoparticles (ZnO NPs) entering the brain via the tongue-brain pathway reduce taste sensitivity and synaptic transmission. This occurs through neuroinflammation mediated by the JAK-STAT pathway, impacting neuronal function and taste perception.

Keywords:
nanoparticlesnerve transportneuroinflammationsynaptic transmissiontaste

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Area of Science:

  • Neuroscience
  • Toxicology
  • Materials Science

Background:

  • Nanoparticles (NPs) can access the brain, particularly via neural pathways, due to their size and bioactivity.
  • Zinc oxide nanoparticles (ZnO NPs) are known to enter the brain through the tongue-brain pathway, but their effects on synaptic transmission and perception remain unclear.

Purpose of the Study:

  • To investigate the impact of tongue-brain transported ZnO NPs on synaptic transmission and taste perception.
  • To elucidate the underlying mechanisms, including neuroinflammation and specific signaling pathways.

Main Methods:

  • Assessed taste sensitivity and learning in the presence of ZnO NPs.
  • Measured miniature excitatory postsynaptic currents, action potential frequency, and c-fos expression.
  • Utilized protein chip arrays to detect inflammatory factors and analyzed the JAK-STAT and Neurexin1-PSD95-Neurologigin1 pathways.

Main Results:

  • Tongue-brain transported ZnO NPs decreased taste sensitivity and learning ability, indicating abnormal taste perception.
  • Synaptic transmission was reduced, evidenced by decreased miniature excitatory postsynaptic currents, action potential frequency, and c-fos expression.
  • Neuroinflammation, originating from neurons, was identified, involving JAK-STAT pathway activation that inhibited the Neurexin1-PSD95-Neurologigin1 pathway and c-fos expression.

Conclusions:

  • ZnO NPs transported via the tongue-brain pathway can induce neuroinflammation and impair synaptic transmission, leading to abnormal taste perception.
  • The JAK-STAT signaling pathway plays a critical role in mediating ZnO NP-induced neuroinflammation and synaptic deficits.
  • Blocking JAK-STAT activation can prevent these adverse effects, highlighting a novel mechanism of NP neurotoxicity.