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Hypotonicity-induced cell swelling activates TRPA1.
Fumitaka Fujita1,2,3, Kunitoshi Uchida4,5, Yasunori Takayama4,5
1Division of Cell Signaling, Okazaki Institute for Integrative Bioscience (National Institute for Physiological Sciences), National Institutes of Natural Sciences, Okazaki, Aichi, 444-8787, Japan. fujita-f@mandom.co.jp.
The Journal of Physiological Sciences : JPS
|June 18, 2017
Summary
Hypotonic solutions cause pain via molecular mechanisms. Researchers found human TRPA1 (hTRPA1) channels activate due to cell swelling, not intracellular calcium changes, clarifying pain pathways.
Area of Science:
- Neuroscience
- Molecular Biology
- Physiology
Background:
- Hypotonic solutions can induce pain in nasal and ocular mucosa.
- The precise molecular mechanisms underlying this pain sensation are not fully understood.
- Transient Receptor Potential Ankyrin 1 (TRPA1) channels are implicated in sensory perception.
Purpose of the Study:
- To investigate the role of human TRPA1 (hTRPA1) in responding to physical stimuli.
- To evaluate the response of hTRPA1 to cell swelling induced by hypotonic conditions.
- To elucidate the molecular mechanisms of pain sensation caused by hypotonic solutions.
Main Methods:
- Utilized Ca2+-imaging techniques to monitor hTRPA1 activity.
- Employed cell-attached patch-clamp recordings to assess single-channel activation.
- Applied hypotonic solutions and specific TRPA1 blockers and modulators (AITC, thapsigargin, BAPTA).
Main Results:
- Hypotonic conditions modulated AITC-induced hTRPA1 activity.
- Cell swelling under hypotonic conditions directly evoked single-channel activation of hTRPA1.
- This activation was inhibited by a known hTRPA1 blocker.
- Intracellular calcium concentration changes were not found to be related to hTRPA1 activation by cell swelling.
Conclusions:
- Human TRPA1 (hTRPA1) channels are activated by physical stimuli, specifically cell swelling.
- Cell swelling-induced hTRPA1 activation is a potential mechanism for pain sensation in hypotonic environments.
- This activation is independent of intracellular calcium level fluctuations.
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