This is consistent with the ability of nVNS to inhibit nociception in models of migraine and other types of headache by stimulating descending inhibitory pain pathways known to be activated by morphine.4,5,40 More specifically, the inhibitory effect of nVNS involved activation of GABAA receptors and 5-HT3 and 5-HT7 receptors in an episodic migraine model.15 Activation of GABAA receptors on primary and second order neurons1,37,55 causes an influx of chloride ions that leads to a hyperpolarized state and blocks neurotransmitter and neuropeptide release. Here, HTR3A is linked to migraine disorder.