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[Abstract Title]. - Society for Neuroscience

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<strong>Title</strong>: Transient receptor potential A1 mediates acetaldehyde-evoked pain sensation<br />

Authors: *S. HWANG, S. BANG, K. KIM, S. YOO;<br />

Grad Sch. Med., Korea Univ., Seoul, Republic of Korea<br />

<strong>Abstract</strong>: Six transient receptor potential (TRP) ion channels expressed in the sensory afferents<br />

are playing an important role as body thermosensors and also peripheral pain detectors. It‟s<br />

known that a number of natural compounds specifically activate those thermo sensitive TRP<br />

channel and a well-known example is cinnamaldehyde <strong>for</strong> TRPA1. Here we show that human<br />

and mouse TRPA1 is activated by acetaldehyde, an intermediate substance of ethanol<br />

metabolism, in HEK293T cell heterologous expression system and culture of mouse trigeminal<br />

neurons. Acetaldehyde failed to activate other temperature-sensitive TRP channels expressed in<br />

sensory neurons. A TRPA1 antagonist camphor and a general TRP blocker ruthenium red<br />

inhibited TRPA1 activation by acetaldehyde. Camphor and ruthenium red also suppressed acute<br />

nociceptive behaviors induced by intradermal administration of acetaldehyde into the mouse<br />

footpad. Intradermal coapplication of prostaglandin E2 with acetaldehyde greatly potentiated the<br />

acetaldehyde-induced nociceptive responses and the effect was reversed by treatment of the<br />

TRPA1 antagonist camphor. These results suggest that acetaldehyde causes nociception via<br />

activation of TRPA1. Our data also may help elucidation of acetaldehyde-related pathological<br />

symptoms such as hangover pain.<br />

Disclosures: S. Hwang , None; S. Bang, None; K. Kim, None; S. Yoo, None.<br />

Poster<br />

265. Nociceptors II<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 265.9/EE10<br />

Topic: D.08.a. Pain transduction molecules and channels<br />

Support: KFO 100/1-2<br />

<strong>Title</strong>: Modulation of TRPV1 activity during Opioid withdrawal<br />

Authors: V. SPAHN, *M. SCHAEFER, C. ZOELLNER;<br />

Anesthesiol and Intensive Care Med., Charité, Campus B. Franklin, Berlin, Germany<br />

<strong>Abstract</strong>: Vanilloid receptor type 1 (TRPV1) is a ligand-gated ion channel expressed on sensory<br />

nerves that responds to noxious heat, protons, and chemical stimuli such as capsaicin. TRPV1<br />

plays a critical role in the development of tissue injury, inflammation or nerve lesions. Opioids

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