Volume 37, Number 1 (Supplement) September 2017 ISSN 0333-1024 (Print) ISSN 1468-2982 (Online) Abstracts of the 18th International Headache Congress International Headache Society 7–10 September 2017 Vancouver Convention Centre Canada www.ihs-headache.org journals.sagepub.com/home/cep Editor-in-Chief, Arne May, Germany Subscriptions and advertising Cephalalgia (ISSN: 0333-1024 print, 1468-2982 online) is published Previous Editors, Ottar Sjaastad (Founding Editor), Marcia Wilkinson, 14 times a year by SAGE Publications Ltd (Los Angeles, London, K Michael Welch, Peter J Goadsby, David W Dodick New Delhi, Singapore, Washington DC and Melbourne). Managing Editor, Wendy Krank The US annual subscription price is [$2539]. Airfreight and mailing in Email: [email protected] the USA by agent Worldnet Shipping Inc., 156-15, 146th Avenue, 2nd Floor, Jamaica, NY 11434, USA. Periodicals postage paid at Jamaica NY Associate Editors 11431. 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View the Cephalalgia Editorial Board confl ict of interest statements here: www.uk.sagepub.com/CEP-ConflictStatements IHC Oral Abstracts Cephalalgia 2017, Vol. 37(1S) 1–24 ! International Headache Society 2017 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/0333102417719571 journals.sagepub.com/home/cep Basic Science more sustained response. CGRP induced Ca2þ increase in some TG neurons, while PACAP induced Ca2þ increase in OC-BA-001 some cells, mostly in glia cells. However, this was observed in very few cells. CGRP and PACAP did not change intra- Characterization of trigeminal ganglion cell cellular calcium in either the GT1-7 cell line or the GH3 spontaneous calcium signalling and responses to cell line. ATP, PACAP and CGRP Conclusion: This result suggests that the different cell Sajedeh Eftekhari1,* and Andrew Charles1 types of TG may be defined based on their spontaneous activity and their intercellular Ca2þ response to ATP. Our 1Neurology, David Geffen School of Medicine at UCLA, Los results also indicate that CGRP and PACAP do not con- Angeles, United States sistently change intracellular Ca2þ in TG cells. Objectives: The trigeminal ganglion (TG) consists of bipolar neurons of different cell sizes and two types of Disclosure of Interest glial cells; satellite glial cells and Schwann cells. The satellite None Declared glial cells surround neuronal cell bodies. The CGRP recep- tor is localized on the large-sized neurons and satellite glial Basic Science cells in rat and human TG. The TG neurons also express PAC1 receptors. It is not known if and how PACAP and OC-BA-002 CGRP effect the calcium signaling in TG. We aimed to characterize the different cell types of TG based on their LOCUS COERULEUS NORADRANERGIC spontaneous calcium signaling activity and responses to PROJECTIONS MODULATE CORTICAL ATP. We also examined the responses of satellite glia SPREADING DEPRESSION THRESHOLDS and neighbouring TG neurons to acute and chronic appli- IN RATS cation of CGRP or PACAP. Marta Vila-Pueyo1,*, Peter J. Goadsby1 Methods: Primary cultures of TG were prepared from and Philip R. Holland1 mice p5-p7. Cultured cells were then loaded with the 1 Ca2þ-specific fluorescent indicator fluo-4AM, and Ca2þ Headache Group, King’s College London, London, responses were quantified using a custom confocal imaging United Kingdom system. Responses of different cell types in the TG culture Objectives: The noradrenergic locus coeruleus (LC) is a to ATP, CGRP or PACAP were analyzed. Parameters quan- key modulator of the sleep-wake cycle, acting as a promo- tified included baseline intracellular calcium, spontaneous ter of arousal. Additionally, noradrenergic projections are calcium transients, and the amplitude and duration of involved in the regulation of cerebral blood flow and LC response to applied ligands. To confirm our results, we stimulation reduces cerebral blood flow. To explore used two different cell lines with spontaneous calcium further a potential role for the LC in migraine pathophy- oscillations; GT1-7 (mouse hypothalamic tumor neurons) siology, we aimed to test whether LC disruption would and GH3 (rat pituitary tumor cells) expressing CGRP and modulate cortical spreading depression (CSD) thresholds. PAC1 receptor. Methods: Sprague-Dawley rats (n ¼ 28) were randomly Results: We have established a cell culture system in treated with vehicle (saline) or N-(2-chloroethyl)-N- which TG neurons develop characteristic cell morphology ethyl-2-bromobenzylamine (DSP4), a selective neurotoxin with extensive processes. Satellite glial cells grow in close that initially induces degeneration of LC noradrenergic contact with the neuronal cell bodies, with morphology axon terminals followed by their cell bodies. Two weeks similar to that observed in vivo. Spontaneous neuronal cal- after treatment, rats were anesthetized with isoflurane and cium transients were observed in neurons and satellite glial maintained with propofol infusion (33–50 mg/kg/h). Two cells, with differences in their temporal and spatial char- cranial windows were drilled in each parietal bone for acteristics. Addition of ATP activated an increase in electrical or chemical induction of CSDs and for DC cor- 2þ [Ca ]I in both neurons and glia, with neurons showing a tical recordings. Following 30 minutes of baseline record- rapid and transient response and glia showing a slower and ings in the left hemisphere, the left cortex was electrically ! International Headache Society 2017 2 Cephalalgia 37(1S) stimulated with increasing electric charge until a CSD was Basic Science induced. Afterwards, baseline recordings were performed for 30 minutes in the right hemisphere, then a cotton ball OC-BA-003 soaked in 1M KCl was placed on the right cortex and CSDs were counted for 1 hour, with KCl refreshed Dissecting Migraine with Optogenetics: every 15 minutes (5 ml). An aversive circuit from the periaqueductal Results: DSP4 treatment resulted in selective loss of gray to the ventral tegmental area 49% (Æ6.5) of the noradrenergic cells in the LC Maggie W. Waung1,* and Howard L. Fields1 (t26 ¼ 5.083, p 0.01) and rats demonstrated a lethargic 1 phenotype. This loss of LC noradrenergic cell bodies was Neurology, University of California San Francisco, associated with an increased propagation of KCl-induced San Francisco, United States CSDs (t23 ¼3.164, p 0.001), more pronouncedly Objectives: Imaging studies of patients