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Molecular battle for neuropathic pain relief...
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cweinbl posted:
TRP ion channels respond to mechanical, thermal, chemical and many other stimuli coming from the extra and intracellular milieu. TRPV1, however, remains the most studied and best characterized TRP family member, due to the fact that it has been implicated in a wide variety of cellular and physiological processes, including noxious physical and chemical stimuli detection, making it a promising target for pain-relieving drugs acting exactly where pain originates.

TRPV1 receptor has been found in both the peripheral and central nervous system within centres
known for their role in pain detection, transmission and regulation, consistent with its key role in
pain. Calcium flowing through TRPV1
channel activates a Ca2+-sensitive PLC, which hydrolyzes PIP2 and leads to its depletion, which in
turn results in diminished channel activity.
TRPV1 receptor is up-regulated in undamaged neurons and down-regulated in damaged ones in several models of neuropathic pain and, interestingly, the increased expression of TRPV1 receptor is related not only to the C-fibers but also to the myelinated A-fibers, which justifies the effectiveness of TRPV1 receptor agonist/antagonists in mechanical allodynia, apart from thermal hyperalgesia (which many of us here have).

Further studies to clarify the role of the supraspinal TRPV1 receptor and in particular, within the antinociceptive descending pathway, may open the way to a novel strategy of pain relief in central nervous system disorders, such as neuropathic pain, which does not yet have an appropriate therapy.

Read the entire article here: http://www.molecularpain.com/content/pdf/1744-8069-6-66.pdf .
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