such as "Introduction", "Conclusion"..etc
February 24, 2009 — Capsaicin, the active
ingredient in spicy hot chili peppers such as the jalapeno, 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.
Capsaicin 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.
"The 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
By 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
"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.
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