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The trigeminovascular system is considered to play a role in the mechanism of migraine headache. Novel in vitro animal models that investigate the release of neuropeptides may be of help to understand the pathophysiology and pharmacology of trigeminal neurons. Here, we examined the release of the immunoreactivity (LI) of the sensory neuropeptides calcitonin gene-related peptide (CGRP) and substance P (SP) from slices of rat and guinea pig trigeminal ganglia with proximal nerve trunks attached. Electrical field stimulation (EFS, 10 Hz), high K+ medium (50 mM) and capsaicin (1 μM) caused a significant increase in CGRP-LI outflow. SP-LI was also released after exposure to EFS, high K+ and capsaicin. The increase in CGRP-LI outflow induced by EFS was markedly reduced in a Ca2+-free medium and by pretreatement with a high capsaicin concentration, tetrodotoxin, ω-conotoxin, dihydroergotamine and sumatriptan. Sensory neuropeptide release from slices of rat trigeminal ganglia with nerve trunks attached fulfills the criteria required to define it as a neurosecretory event. This is a novel method for studying trigeminal neuron pathophysiology and the action of antimigraine drugs.

Neuropeptide release from slices of rat and guinea pig trigeminal ganglia: modulation by dihydroergotamine and sumatriptan