Your privacy, your choice

We use essential cookies to make sure the site can function. We also use optional cookies for advertising, personalisation of content, usage analysis, and social media.

By accepting optional cookies, you consent to the processing of your personal data - including transfers to third parties. Some third parties are outside of the European Economic Area, with varying standards of data protection.

See our privacy policy for more information on the use of your personal data.

for further information and to change your choices.

Skip to main content
Fig. 3 | The Journal of Headache and Pain

Fig. 3

From: Hypersensitivity to BKCa channel opening in persistent post-traumatic headache

Fig. 3

Possible Mechanisms and Sites of Action of Migraine-Like Headache induced by BKCa Channel Opening in Persons with PPTH. The figure outlines a proposed mechanism and site of action though which opening of BKCa channels contributes to the development of migraine-like headache in persons with PPTH. In this suggested model, the signaling molecules CGRP and PACAP-38 bind to their respective G protein-coupled receptors present on the vascular smooth muscle cells of intracranial arteries. This initiates the activation of cAMP-dependent signaling pathways, which then results in opening of BKCa channels. The subsequent release of potassium ions and accompanying vasodilation leads to activation and sensitization of perivascular meningeal nociceptors, a process facilitated by both chemical and mechanical stimulation. Modified from Al-Khazali et al., 2023 [21]. CGRP = calcitonin gene-related peptide; PACAP-38 = pituitary adenylate cyclase-activating polypeptide-38; AC = adenylate cyclase; ATP = adenosine triphosphate; cAMP = cyclic adenosine monophosphate; BKCa channels = large conductance calcium-activated potassium channels

Back to article page