Trigeminal ganglion neurons are directly activated by influx of CSF solutes in a migraine model
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Trigeminal ganglion neurons are directly activated by influx of CSF solutes in a migraine model. / Kaag Rasmussen, Martin; Møllgård, Kjeld; Bork, Peter A R; Weikop, Pia; Esmail, Tina; Drici, Lylia; Wewer Albrechtsen, Nicolai J; Carlsen, Jonathan Frederik; Huynh, Nguyen P T; Ghitani, Nima; Mann, Matthias; Goldman, Steven A; Mori, Yuki; Chesler, Alexander T; Nedergaard, Maiken.
In: Science (New York, N.Y.), Vol. 385, No. 6704, 2024, p. 80-86.Research output: Contribution to journal › Journal article › Research › peer-review
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TY - JOUR
T1 - Trigeminal ganglion neurons are directly activated by influx of CSF solutes in a migraine model
AU - Kaag Rasmussen, Martin
AU - Møllgård, Kjeld
AU - Bork, Peter A R
AU - Weikop, Pia
AU - Esmail, Tina
AU - Drici, Lylia
AU - Wewer Albrechtsen, Nicolai J
AU - Carlsen, Jonathan Frederik
AU - Huynh, Nguyen P T
AU - Ghitani, Nima
AU - Mann, Matthias
AU - Goldman, Steven A
AU - Mori, Yuki
AU - Chesler, Alexander T
AU - Nedergaard, Maiken
PY - 2024
Y1 - 2024
N2 - 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.
AB - 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.
KW - Animals
KW - Mice
KW - Calcitonin Gene-Related Peptide/cerebrospinal fluid
KW - Cerebrospinal Fluid/metabolism
KW - Cortical Spreading Depression
KW - Disease Models, Animal
KW - Migraine Disorders/cerebrospinal fluid
KW - Proteome/metabolism
KW - Signal Transduction
KW - Trigeminal Ganglion/metabolism
U2 - 10.1126/science.adl0544
DO - 10.1126/science.adl0544
M3 - Journal article
C2 - 38963846
VL - 385
SP - 80
EP - 86
JO - Science
JF - Science
SN - 0036-8075
IS - 6704
ER -
ID: 397721692