Abstract
BackgroundMigraine and Cluster Headache (CH) are two primary headaches with severe disease burden. The disease expression and the mechanisms involved are poorly known. In some attacks of migraine and in most attacks of CH, there is a release of vasoactive intestinal peptide (VIP) originating from parasympathetic cranial ganglia such as the sphenopalatine ganglion (SPG). Patients suffering from these diseases are often deprived of effective drugs. The aim of the study was to examine the localization of the botulinum toxin receptor element synaptic vesicle glycoprotein 2A (SV-2A) and the vesicular docking protein synaptosomal-associated protein 25 (SNAP25) in human and rat SPG. Additionally the expression of the neurotransmitters pituitary adenylate cyclase activating polypeptide (PACAP-38), nitric oxide synthase (nNOS), VIP and 5-hydroxttryptamine subtype receptors (5-HT1B,1D,1F) were examined.MethodsSPG from adult male rats and from humans, the later removed at autopsy, were prepared for immunohistochemistry using specific antibodies against neurotransmitters, 5-HT1B,1D,1F receptors, and botulinum toxin receptor elements.ResultsWe found that the selected neurotransmitters and 5-HT receptors were expressed in rat and human SPG. In addition, we found SV2-A and SNAP25 expression in both rat and human SPG. We report that all three 5-HT receptors studied occur in neurons and satellite glial cells (SGCs) of the SPG. 5-HT1B receptors were in addition found in the walls of intraganglionic blood vessels.ConclusionsRecent focus on the SPG has emphasized the role of parasympathetic mechanisms in the pathophysiology of mainly CH. The development of next generation’s drugs and treatment of cranial parasympathetic symptoms, mediated through the SPG, can be modulated by treatment with BoNT-A and 5-HT receptor agonists.
Highlights
Migraine and Cluster Headache (CH) are two primary headaches with severe disease burden
The aim of the present work was to examine if rat and human sphenopalatine ganglion (SPG) contain the SV2-A and synaptosomal-associated protein 25 (SNAP25) proteins and, by extension, if BoNT-A might have a mechanism of action in SPG
PACAP-38 immunoreactivity was found in the satellite glial cells (SGCs) in all animals (Fig. 2a). nNOS was expressed in the cytoplasm of the neurons and in intraganglionic nerve fibers in a pearllike manner around the neurons (Figs. 2b)
Summary
Migraine and Cluster Headache (CH) are two primary headaches with severe disease burden. In some attacks of migraine and in most attacks of CH, there is a release of vasoactive intestinal peptide (VIP) originating from parasympathetic cranial ganglia such as the sphenopalatine ganglion (SPG). Patients suffering from these diseases are often deprived of effective drugs. Raised levels of VIP and, in particular, calcitonin gene-related protein (CGRP) have been measured during spontaneous CH attacks These findings were considered as evidence of involvement of the cranial parasympathetic nervous system [2]. In human SPG the parasympathetic signaling transmitters in neural cell bodies consist mainly of VIP, PACAP, acetylcholine (ACh) and NOS [10]
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