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PDE9A, PDE10A, and PDE11A expression in rat trigeminovascular pain signalling system: role in pathogenesis of migraine?
© Kruse et al; licensee BioMed Central Ltd. 2007
Published: 25 July 2007
Activation of the trigeminovascular pain signalling system, which includes cerebral arteries, meninges, trigeminal ganglion, and brain stem, may be involved in migraine. Furthermore, stimulation of cyclic nucleotide (cAMP and cGMP) production as well as inhibition of phosphodiesterases (PDEs) induces headache and migraine [1–4]. The aim is to study the expression of the most recently discovered PDE subtypes (9A, 10A and 11A) in cerebral arteries, the dura mater, and the trigeminal ganglion and nucleus. This may give a clue to a role in pathogenesis of migraine.
The amount of mRNA and protein in the middle cerebral artery, basilar artery, dura, trigeminal ganglion, and caudal trigeminal nucleus of male Sprague-Dawley rats were investigated using real-time PCR, Western blot, and immunohistochemistry, and compared to two peripheral arteries: aorta and mesenteric artery, as well as neocortex and cerebellum.
We here present, for the first time the expression of the three most recently discovered PDEs in the trigeminovascular pain signalling system. The functional implications are yet unknown, but their localisation indicates that PDE9A, PDE10A and PDE11A may have a role in pathogenesis of migraine.
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