Up-regulation of 5-HT2 Serotonin Receptor: A Possible Mechanism of Transformed Migraine

Authors

  • Anan Srikiatkhachorn M.D.,

    Corresponding author
    1. Neuro- and Behavioural Biology Center, Institute of Science and Technology for Development, Mahidol University, Salaya, Nakornpathom 73170, Thailand
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  • Piyarat Govitrapong Ph.D.,

    1. Neuro- and Behavioural Biology Center, Institute of Science and Technology for Development, Mahidol University, Salaya, Nakornpathom 73170, Thailand
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  • Chanchira Limthavon M.S.

    1. Neuro- and Behavioural Biology Center, Institute of Science and Technology for Development, Mahidol University, Salaya, Nakornpathom 73170, Thailand
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Address all correspondence to: Anan Srikiatkhachorn, M.D., Neuro- and Behavioural Biology Center, Institute of Science and Technology for Development, Mahidol University, Salaya, Nakornpathom 73170, Thailand

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-HT2 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. [3H]-spiperone and ketanserin were used to determine the specific binding. We found a significant increase (P <0.05) in the maximal receptor numbers (Bmax ) 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.

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