Fig. 2
From: The big CGRP flood - sources, sinks and signalling sites in the trigeminovascular system
Scheme of signalling sites for CGRP in the trigeminovascular system. In the trigeminal ganglion (a) CGRP released from neurons may signal to neighbouring neurons, glial satellite cells (GSC) and possibly Schwann cells (SC) expressing CGRP receptors and can thus, via gene expression, influence the production of substances, e.g. nitric oxide (NO), brain-derived neurotrophic factor (BDNF) and CGRP receptor components. These (NO) may signal back to the neurons, or (BDNF, CGRP receptors) may be transported through the central extensions of trigeminal afferents (Aδ/C) to the spinal trigeminal nucleus. CGRP signalling at arterial vessels, e.g. the pial vessels of the spinal medulla (b), causes vasodilatation and increased blood flow. Within the spinal trigeminal nucleus (c) CGRP is released from central terminals of trigeminal afferents and signals most likely to other central terminals equipped with CGRP receptors, which may lead to increased neurotransmitter (glutamate) release and facilitation of nociceptive transmission. Release of BDNF may pre- and postsynaptically potentiate synaptic transmission. Neurons with inhibitory neurotransmitters (GABA) may counteract the pronociceptive synaptic processes