What question did this study set out to answer?

To determine the molecular mechanism and functional role of Mas-related GPCR D (MrgprD) in chronic constriction injury-induced neuropathic pain.

August 27, 2018The FASEB JournalOpen Access

Facilitation of MrgprD by TRP‐A1 promotes neuropathic pain

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Authors

CWChangming Wang LGLeying Gu YRYonglan Ruan

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Overview

Preclinical study reveals that TRPA1 facilitates MrgprD activation to drive cold allodynia in nerve injury models, highlighting a potential therapeutic target for neuropathic pain.

Key Points

To determine the molecular mechanism and functional role of Mas-related GPCR D (MrgprD) in chronic constriction injury-induced neuropathic pain.
Evaluated mechanical, cold, and heat sensitivity behaviors alongside itch responses in rodent models subjected to chronic constriction injury (CCI).
Measured β-alanine-evoked calcium signaling and downstream PKA signaling pathways in dorsal root ganglion neurons and co-transfected HEK293 cells.
Assessed pain responses in TRPA1 knockout models following nerve injury and β-alanine stimulation.
MrgprD is specifically required for the induction of mechanical hypersensitivity and cold allodynia, without altering heat allodynia.
TRPA1 functions downstream of MrgprD, mediating β-alanine-induced calcium influx via PKA pathway activation in sensory neurons and cell models.
Nerve-injured models exhibited heightened β-alanine-induced pain behavior while itch responses remained unaltered, and TRPA1 knockout significantly attenuated this pain response.

Cite This Study

Wang et al. (2018) studied this question.

synapsesocial.com/papers/6aaa2db32f1eb85158fcab6a https://doi.org/10.1096/fj.201800615rr

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August 27, 2018The FASEB JournalOpen Access

Facilitation of MrgprD by TRP‐A1 promotes neuropathic pain

View Full Paper

Ask AI

Bookmark

Authors

CWChangming Wang LGLeying Gu YRYonglan Ruan

Discussion

Member takes

Overview

Preclinical study reveals that TRPA1 facilitates MrgprD activation to drive cold allodynia in nerve injury models, highlighting a potential therapeutic target for neuropathic pain.

Key Points

To determine the molecular mechanism and functional role of Mas-related GPCR D (MrgprD) in chronic constriction injury-induced neuropathic pain.
Evaluated mechanical, cold, and heat sensitivity behaviors alongside itch responses in rodent models subjected to chronic constriction injury (CCI).
Measured β-alanine-evoked calcium signaling and downstream PKA signaling pathways in dorsal root ganglion neurons and co-transfected HEK293 cells.
Assessed pain responses in TRPA1 knockout models following nerve injury and β-alanine stimulation.
MrgprD is specifically required for the induction of mechanical hypersensitivity and cold allodynia, without altering heat allodynia.
TRPA1 functions downstream of MrgprD, mediating β-alanine-induced calcium influx via PKA pathway activation in sensory neurons and cell models.
Nerve-injured models exhibited heightened β-alanine-induced pain behavior while itch responses remained unaltered, and TRPA1 knockout significantly attenuated this pain response.

Cite This Study

Wang et al. (2018) studied this question.

synapsesocial.com/papers/6aaa2db32f1eb85158fcab6a https://doi.org/10.1096/fj.201800615rr

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