Abstract
TRPA1 receptor channels are activated by environmental irritants and by endogenous mediators released during inflammatory conditions ( McMahon & Wood 2006 ). Activation of TRPA1 receptors causes CGRP release from trigeminal ganglion neurons and increases meningeal blood flow upon nasal stimulation ( Kunkler et al. 2011 ), providing evidence that TRPA1 receptors may be involved in the generation of headaches.
Highlights
TRPA1 receptor channels are activated by environmental irritants and by endogenous mediators released during inflammatory conditions (McMahon & Wood 2006,)
Acrolein significantly stimulated calcitonin generelated peptide (CGRP) release from the dura mater within 5 min and increased meningeal blood flow. Both responses were suppressed by the TRPA1 inhibitor HC030031
To further examine the role of TRPA1 receptor activation in processes presumably associated with headache generation, we investigated the effects of the TRPA1 agonist acrolein on functions involved in meningeal nociception using four different rat models
Summary
TRPA1 receptor channels are activated by environmental irritants and by endogenous mediators released during inflammatory conditions (McMahon & Wood 2006,). Results Acrolein did not elicit discharges in meningeal Aδ- or C-fibres in the hemisected cranial preparation and did not change the discharge activity of second order neurons with meningeal receptive fields in anaesthetized animals.
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