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Review
. 2015 Sep;11(3):307-16.
doi: 10.1007/s11302-015-9453-8. Epub 2015 May 10.

The role of purinergic signaling in the etiology of migraine and novel antimigraine treatment

Marek Cieślak  1 , Joanna Czarnecka, Katarzyna Roszek, Michał Komoszyński
Affiliations
Review

The role of purinergic signaling in the etiology of migraine and novel antimigraine treatment

Marek Cieślak et al. Purinergic Signal. 2015 Sep.

Abstract

Etiopathogenesis of migraine involves different structures of the central nervous system: the trigeminal nerve with nuclei located in the brain stem, vascular system, and the cerebral cortex as well as diverse mechanisms and pathological processes. The multidirectional action of purines in different cell types (blood vessels, neurons, and satellite glial cells) and through different types of purinergic receptors contributes to the etiopathogenesis of migraine pain. Adenosine triphosphate (ATP) and its derivatives are involved in initiation and propagation of migrenogenic signals in several ways: they participate in vasomotor mechanism, cortical spreading depression, and in fast transmission or cross-excitation based on the satellite glial cells in trigeminal ganglion. Contribution of purinergic signaling in the conduction of pain is realized through the activation of P1 and P2 receptors expressed widely in the central nervous system: on the neurons and glial cells as well as on the smooth muscles and endothelium in the vascular system. Therefore, the purinergic receptors can be an excellent target for pharmacologists constructing new antimigraine therapeutics. Moreover, the mechanisms facilitating ATP and adenosine degradation may prevent vasodilatation and thus avoid a secondary central sensitization during a migraine attack. Thus, agonists and antagonists of P receptors as well as ecto-enzymes metabolizing nucleotides/nucleosides could gain the growing attention as therapeutic agents.

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Figures

Fig. 1
Fig. 1
The dual role of ATP involved in vasomotor etiology of migraine attack
Fig. 2
Fig. 2
Propagation of pain signal within the trigeminal ganglion (“cross-excitation”). Excitation potentials of neurons cause an increase in ATP release outside the cell. ATP activates P2X receptors on the postsynaptic cell membranes, as well as P2Y receptors on satellite glial cells (SGCs). ATP released from neurons and satellite glial cells causes the spread of Ca2+ waves in the neighboring cells, and the excitation spreads out
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