Trigeminal ganglion neuron subtype‐specific alterations of CaV2.1 calcium current and excitability in a Cacna1a mouse model of migraine

B. Fioretti; L. Catacuzzeno; L. Sforna; M. B. Gerke‐Duncan; A. M. J. M. van den Maagdenberg; F. Franciolini; M. Connor; D. Pietrobon

doi:10.1113/jphysiol.2011.220533

journal article Nov 29, 2011

Trigeminal ganglion neuron subtype‐specific alterations of CaV2.1 calcium current and excitability in a Cacna1a mouse model of migraine

B. Fioretti L. Catacuzzeno L. Sforna M. B. Gerke‐Duncan A. M. J. M. van den Maagdenberg F. Franciolini M. Connor

D. Pietrobon

The Journal of Physiology Vol. 589 No. 23 pp. 5879-5895 · Wiley

View at Publisher Save 10.1113/jphysiol.2011.220533

Abstract

Non‐technical summary Activation of trigeminal neurons innervating the meninges and release of proinflammatory peptides (in particular calcitonin gene‐related peptide (CGRP)) from their terminals are believed to play a key role in generating migraine pain. A monogenic subtype of migraine (familial hemiplegic migraine type‐1 (FHM1)) is caused by gain‐of‐function mutations in a neuronal voltage‐gated calcium channel (Cav2.1) involved in controlling neurotransmitter release from many synaptic terminals including those of trigeminal neurons at the meninges. Using a FHM1 transgenic mouse model, we show that the migraine mutation produces gain‐of‐function (i.e. it increases calcium influx) in a subpopulation of trigeminal neurons that do not innervate the meninges. In contrast, the calcium channels of trigeminal neurons innervating the meninges and releasing CGRP are not affected by the mutation. Congruently, the migraine mutation does not alter CGRP release at the meninges. Our findings suggest that the facilitation of CGRP actions at the meninges does not contribute to the generation of headache in FHM1.

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Details

Published: Nov 29, 2011
Vol/Issue: 589(23)
Pages: 5879-5895
License: View

Authors

A. M. J. M. van den Maagdenberg

Cite This Article

B. Fioretti, L. Catacuzzeno, L. Sforna, et al. (2011). Trigeminal ganglion neuron subtype‐specific alterations of CaV2.1 calcium current and excitability in a Cacna1a mouse model of migraine. The Journal of Physiology, 589(23), 5879-5895. https://doi.org/10.1113/jphysiol.2011.220533

Trigeminal ganglion neuron subtype‐specific alterations of CaV2.1 calcium current and excitability in a Cacna1a mouse model of migraine

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