Peripheral sensitization in migraine—role for P2X purinergic receptors in the dura–vascular sensory pathway

Jennings, Ernest A., and Cho, Hyun-jung (2007) Peripheral sensitization in migraine—role for P2X purinergic receptors in the dura–vascular sensory pathway. Drug Development Research, 68 (6). pp. 321-328.

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Abstract

Peripheral sensitization is still considered a prime contributor underlying the mechanisms of migraine. Trigeminal primary afferent neurons are the first neurons in the dural nociceptive pathway, and activation results in conscious perception of pain. Peripheral sensitization can lower the activation threshold of primary afferent neurons, rendering them more excitable, allowing for increases in release of neurotransmitter from both central and peripheral terminals. Increase in neurotransmitter release from central terminals contributes to excitation of second-order neurons, while the release of peptides from peripheral terminals has been implicated in neurogenic inflammation. Adenosine 5'-triphosphate (ATP) causes pain in human studies, and depolarize sensory neurons. There is evidence of the action of ATP at many levels in the dura–vascular sensory pathway. Animal studies have shown that some P2X receptors are located in neurons innervating the dura, including the P2X3 receptor, which is most often shown to be involved in nociceptive pathways. In this article, we briefly review peripheral sensitization in relation to migraine and provide emphasis for P2X receptor involvement where it is available.

Item ID: 17685
Item Type: Article (Refereed Research - C1)
Keywords: migraine, trigeminal, P2X, ATP, pain
ISSN: 1098-2299
Date Deposited: 04 Aug 2011 04:03
FoR Codes: 11 MEDICAL AND HEALTH SCIENCES > 1115 Pharmacology and Pharmaceutical Sciences > 111502 Clinical Pharmacology and Therapeutics @ 50%
11 MEDICAL AND HEALTH SCIENCES > 1109 Neurosciences > 110906 Sensory Systems @ 50%
SEO Codes: 92 HEALTH > 9201 Clinical Health (Organs, Diseases and Abnormal Conditions) > 920111 Nervous System and Disorders @ 100%
Citation Count from Web of Science Web of Science 2
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