Publication: Up‐regulation of 5‐HT<inf>2</inf> Serotonin Receptor: A Possible Mechanism of Transformed Migraine
Issued Date
1994-01-01
Resource Type
ISSN
15264610
00178748
00178748
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2-s2.0-0028175480
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Mahidol University
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SCOPUS
Bibliographic Citation
Headache: The Journal of Head and Face Pain. Vol.34, No.1 (1994), 8-11
Suggested Citation
Anan Srikiatkhachorn, Piyarat Govitrapong, Chanchira Limthavon Up‐regulation of 5‐HT<inf>2</inf> Serotonin Receptor: A Possible Mechanism of Transformed Migraine. Headache: The Journal of Head and Face Pain. Vol.34, No.1 (1994), 8-11. doi:10.1111/j.1526-4610.1994.hed3401008.x Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/9753
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Title
Up‐regulation of 5‐HT<inf>2</inf> Serotonin Receptor: A Possible Mechanism of Transformed Migraine
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Abstract
SYNOPSIS Transformation of episodic migraine to chronic daily headache (so called transformed migraine) ia now a well recognized phenomenon. Although several factors, i.e. analgesic overuse, increasing age, psychiatric disorders are reported to play some roles in this transformation, the precise cascade is still unclear. Further suppression of an already abnormal antinociceptive system with up‐regulation of post‐synaptic receptors is one of the possible explanation. In order to understand the mechanism underlying this condition, 5‐HT 2 serotonin receptors on platelets were assayed by the radioligand binding technique. Six transformed migraine patients (67.67 ± 1.52 years) and seven healthy controls (72.86 ± 1.82 years) were studied. [ 3 H]‐spiperone and ketanserin were used to determine the specific binding. We found a significant increase (P < 0.05) in the maximal receptor numbers (B max ) on platelet membrane of the migraine patients when compared to the controls (64.31 ± 11.06 end 39.96 ± 5.42 fmol/mg protein, respectively), whereas the dissociation equilibrium constant (K D ) values remained unchanged (3.63 ± 0.78 nM and 2.84 ± 0.48 nM for the migraine patients and controls, respectively). The up‐regulation of serotonin receptors found in this study provided further support to the ”serotonergic hypofunction“ theory of migraine pathogenesis and may explain the unusual loss of episodicity seen in the transformed migraine patients. Copyright © 1994, Wiley Blackwell. All rights reserved