Contact: Sally Hubbard
Public Library of Science
Chili peppers help to unravel the mechanism of pain
Press release from PLoS Biology
the active ingredient in chili peppers, is most often experienced as an
irritant, but it may also be used to reduce pain. A new work published
by Drs. Feng Qin and Jing Yao in this week's
PLoS Biology uses
capsaicin to uncover novel insight into how pain-receptor systems can
adapt to painful stimuli. Sensory systems are well known to adapt to
prevailing stimuli. For example, adaptation happens when your eyes
adjust from a dark movie theater during a matinee to the bright
sunlight outside. Whether pain receptors truly adapt or rescale their
responses (versus simply desensitizing) has been an open question.
acts by binding to a receptor in the cell wall of nerve endings and
triggering an influx of calcium ions into the neuron. Eventually, the
nervous system interprets this cascade of events as pain or heat,
depending on which nerves are stimulated. Scientists had previously
linked the pain-relieving effects of capsaicin to a lipid called PIP2,
found in cell membranes. When capsaicin is applied to the skin it
induces a strong depletion of PIP2 in the cell membrane.
receptor acts like a gate to the neurons," said Qin. "When stimulated
it opens, letting outside calcium enter the cells until the receptor
shuts down, a process called desensitization. The analgesic action of
capsaicin is believed to involve this desensitization process. However,
how the entry of calcium leads to the loss of sensitivity of the
neurons was not clear."
Capsaicin creams are commonly sold
over the counter as effective treatment for a variety of pain
syndromes, from minor muscle or joint aches to those that are very
difficult to treat, such as arthritis and neuropathic pain.
combining electrical and optical measurements, the authors now have
been able to link directly the depletion of PIP2 and the
desensitization of the receptor. The authors also showed that the
receptor is fully functional after desensitization – i.e. although you
stop feeling pain – are desensitized – if another event occurs that
would normally trigger a 'pain' response – such as an increased
concentration of capsaicin - the desensitization does not affect that
feeling. "What changed was the responsiveness threshold," said Qin. "In
other words, the receptor had not desensitized per se, but its
responsiveness range was shifted. This property, called adaptation,
would allow the receptor to continuously respond to varying stimuli
over a large capsaicin concentration range."
The findings have
implications for pain sensation mechanisms as well as clinical
applications. With an adaptive response, the receptors are essentially
autoregulated without a fixed threshold, thus the intensity of the pain
you experience is dependent on the recent history of pain.
Yao J, Qin F (2009) Interaction with phosphoinositides confers
adaptation onto the TRPV1pain receptor. PLoS Biol 7(2): e1000046.
PLEASE ADD THE LINK TO THE PUBLISHED ARTICLE IN ONLINE VERSIONS OF YOUR REPORT: http://biology.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pbio.1000046
PRESS ONLY PREVIEW OF THE ARTICLE: http://www.plos.org/press/plbi-07-02-Qin.pdf
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Departments of Physiology and Biophysics
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