Trigeminal ganglion neurons are directly activated by influx of CSF solutes in a migraine model-Reference-Cited by-同舟云学术

Trigeminal ganglion neurons are directly activated by influx of CSF solutes in a migraine model

Published:2024-07-05 Issue:6704 Volume:385 Page:80-86
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Kaag Rasmussen Martin¹^ORCID,Møllgård Kjeld²^ORCID,Bork Peter A. R.¹^ORCID,Weikop Pia¹,Esmail Tina¹^ORCID,Drici Lylia³^ORCID,Wewer Albrechtsen Nicolai J.³⁴^ORCID,Carlsen Jonathan Frederik⁵⁶^ORCID,Huynh Nguyen P. T.⁷⁸^ORCID,Ghitani Nima⁹^ORCID,Mann Matthias³¹⁰,Goldman Steven A.¹⁷⁸^ORCID,Mori Yuki¹^ORCID,Chesler Alexander T.⁹¹¹^ORCID,Nedergaard Maiken¹⁷^ORCID

Affiliation:

1. Center for Translational Neuromedicine, University of Copenhagen, 2200 Copenhagen, Denmark.

2. Department of Cellular and Molecular Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.

3. NNF Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.

4. Department for Clinical Biochemistry, University Hospital Copenhagen - Bispebjerg, Copenhagen, 2400 Copenhagen, Denmark.

5. Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, 2200 Copenhagen, Denmark.

6. Department of Radiology, Copenhagen University Hospital-Rigshospitalet, 2100 Copenhagen, Denmark.

7. Center for Translational Neuromedicine, Division of Glial Disease and Therapeutics, University of Rochester Medical Center, Rochester, NY 14642, USA.

8. Sana Biotechnology, Cambridge, MA 02139, USA.

9. National Center for Complementary and Integrative Health (NCCIH), Bethesda, MD 20892, USA.

10. Department of Proteomics and Signal Transduction, Max-Planck Institute of Biochemistry, 82152 Martinsried, Germany.

11. National Institute of Neurological Disorders and Stroke, Bethesda, MD 20892, USA.

Abstract

Classical migraine patients experience aura, which is transient neurological deficits associated with cortical spreading depression (CSD), preceding headache attacks. It is not currently understood how a pathological event in cortex can affect peripheral sensory neurons. In this study, we show that cerebrospinal fluid (CSF) flows into the trigeminal ganglion, establishing nonsynaptic signaling between brain and trigeminal cells. After CSD, ~11% of the CSF proteome is altered, with up-regulation of proteins that directly activate receptors in the trigeminal ganglion. CSF collected from animals exposed to CSD activates trigeminal neurons in naïve mice in part by CSF-borne calcitonin gene–related peptide (CGRP). We identify a communication pathway between the central and peripheral nervous system that might explain the relationship between migrainous aura and headache.

Publisher

American Association for the Advancement of Science (AAAS)

Link

https://www.science.org/doi/pdf/10.1126/science.adl0544

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