Abstract
Activation of TRPA1 receptors has recently been shown to cause release of calcitonin gene-related peptide (CGRP) from trigeminal ganglion neurons and to increase meningeal blood flow in animals ( Kunkler et al. 2011 ), events regarded to be associated with headaches. Meningeal blood flow is also increased by donors of nitric oxide (NO), partly mediated by the release of CGRP from meningeal afferents ( Strecker et al. 2002 ).
Highlights
Activation of TRPA1 receptors has recently been shown to cause release of calcitonin gene-related peptide (CGRP) from trigeminal ganglion neurons and to increase meningeal blood flow in animals (Kunkler et al 2011,), events regarded to be associated with headaches
Considering this possibility we examined the role of nitric oxide (NO)-/HNO in a rat model of meningeal blood flow
TRPA1 receptor immunoreactivity was found in a proportion of small trigeminal ganglion neurons
Summary
Activation of TRPA1 receptors has recently been shown to cause release of calcitonin gene-related peptide (CGRP) from trigeminal ganglion neurons and to increase meningeal blood flow in animals (Kunkler et al 2011,), events regarded to be associated with headaches. Meningeal blood flow is increased by donors of nitric oxide (NO), partly mediated by the release of CGRP from meningeal afferents (Strecker et al 2002)
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