Tongue-Brain-Transported ZnO Nanoparticles Induce Abnormal Taste Perception

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.