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Pain
is always unpleasant; but it is nonetheless necessary for
our survival. Preliminary pain can serve to indicate that
an injury is pending. After an initial attack, pain can protect
an injured region from further damage and therefore help the
healing process. In this sense, pain is beneficiary. It is
a critical component of our defense system.
Accomplishing
the sensation of pain is no simple feat. It involves both
peripheral and central nerve system as well as interactions
with the immune system among others. The initial perception
of pain occurs at the site of so-called nociceptors, a set
of neurons that are specialized in detection of harmful events.
Distinct from other sensations, nociception is responsive
to a diversity of stimulus that may arise from any origin,
while being able to distinguish them between being nocuous
and innocuous. Two groups of nociceptors can be distinguished.
One group, the medium-diameter, lightly myelinated Ad fibers,
are devoted to intense mechanical deformation. The other,
the small-diameter, unmyekinated C fibers, are polymodal and
sensitive to thermal, mechanical, or chemical stimulus in
noxious ranges as well as thermal perturbations in the non-noxious
range. Intermixed together, these neurons project their axons
into the spinal cord and transmit their signals into the brain
for the interpretation of pain.
Our
lab is primarily interested in nociceptive ion channels that
transduce noxious stimuli into electrical events. Of particular
interest is the thermal receptors that can be activated by
temperature. Study of these receptors will not only help elucidating
the mechanism of thermal sensation, but also provide insights
into the biophysical and structural basis of thermal sensitivity
of ion channel proteins.
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