Warmth Suppresses and Desensitizes Damage-Sensing Ion Channel TRPA1

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چکیده

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Warmth suppresses and desensitizes damage-sensing ion channel TRPA1

BACKGROUND Acute or chronic tissue damage induces an inflammatory response accompanied by pain and alterations in local tissue temperature. Recent studies revealed that the transient receptor potential A1 (TRPA1) channel is activated by a wide variety of substances that are released following tissue damage to evoke nociception and neurogenic inflammation. Although the effects of a noxious range...

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Zinc activates damage-sensing TRPA1 ion channels.

Zinc is an essential biological trace element. It is required for the structure or function of over 300 proteins, and it is increasingly recognized for its role in cell signaling. However, high concentrations of zinc have cytotoxic effects, and overexposure to zinc can cause pain and inflammation through unknown mechanisms. Here we show that zinc excites nociceptive somatosensory neurons and ca...

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Supercooling Agent Icilin Blocks a Warmth-Sensing Ion Channel TRPV3

Transient receptor potential vanilloid subtype 3 (TRPV3) is a thermosensitive ion channel expressed in a variety of neural cells and in keratinocytes. It is activated by warmth (33-39°C), and its responsiveness is dramatically increased at nociceptive temperatures greater than 40°C. Monoterpenoids and 2-APB are chemical activators of TRPV3 channels. We found that Icilin, a known cooling substan...

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Using Neurogenetics and the Warmth-Gated Ion Channel TRPA1 to Study the Neural Basis of Behavior in Drosophila

Here we describe a set of straightforward laboratory exercises that integrate the study of genetics, neuroanatomy, cellular physiology and animal behavior. We use genetic tools in Drosophila for visualizing and remotely activating ensembles of neurons with heat pulses. First, we show how to examine the anatomy of several neuronal populations using genetically encoded green fluorescent protein. ...

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An ion channel essential for sensing chemical damage.

Tissue damage and its downstream consequences are experimentally assayed by formaldehyde application, which indiscriminately modifies proteins and is presumed to cause pain through broadly acting mechanisms. Here we show that formaldehyde activates the ion channel TRPA1 and that TRPA1-deficient mice exhibit dramatically reduced formaldehyde-induced pain responses. 4-Hydroxynonenal, a reactive c...

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ژورنال

عنوان ژورنال: Molecular Pain

سال: 2012

ISSN: 1744-8069,1744-8069

DOI: 10.1186/1744-8069-8-22