Abstract
Extracellular signal-regulated kinase (ERK) is known to be phosphorylated after exposure to noxious stimuli. In this study, we investigated the response in the dura mater to nociceptive stimulation, which is thought to be responsible for the pathogenesis of headaches, including migraines. We also examined the level of ERK phosphorylation in the trigeminal ganglion following cortical spreading depression (CSD), which is thought to play an important role in migraine pathophysiology. Western blot and immunohistochemical analyses showed a significant increase in the ERK phosphorylation levels 3. min following an application of 10. mM capsaicin to the dura mater. This increase was inhibited after an application of the TRPV1 antagonist capsazepine or a MEK inhibitor. An immunohistochemical analysis revealed that most of the small-sized trigeminal ganglion neurons with TRPV1-immunoreactivity that innervate the dura mater exhibited pERK-immunoreactivity, suggesting that these neurons had responded to nociceptive stimulation. CSD increased the level of ERK phosphorylation 30. min after its elicitation, and this response was inhibited by a prior intraventricular administration of TRPV1 antagonist. These results indicate that CSD can activate dural TRPV1 to send nociceptive signals to the trigeminal system, and they provide important clues regarding the relationship between CSD and the trigeminovascular system.
| Original language | English |
|---|---|
| Pages (from-to) | 110-119 |
| Number of pages | 10 |
| Journal | Neuroscience Research |
| Volume | 77 |
| Issue number | 1-2 |
| DOIs | |
| Publication status | Published - 2013 Sep |
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Keywords
- Cortical spreading depression
- ERK
- Trigeminal ganglion
- TRPV1
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
Activation of extracellular signal-regulated kinase in the trigeminal ganglion following both treatment of the dura mater with capsaicin and cortical spreading depression. / Iwashita, Tatsuo; Shimizu, Toshihiko; Shibata, Mamoru; Toriumi, Haruki; Ebine, Taeko; Funakubo, Megumi; Suzuki, Norihiro.
In: Neuroscience Research, Vol. 77, No. 1-2, 09.2013, p. 110-119.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Activation of extracellular signal-regulated kinase in the trigeminal ganglion following both treatment of the dura mater with capsaicin and cortical spreading depression
AU - Iwashita, Tatsuo
AU - Shimizu, Toshihiko
AU - Shibata, Mamoru
AU - Toriumi, Haruki
AU - Ebine, Taeko
AU - Funakubo, Megumi
AU - Suzuki, Norihiro
PY - 2013/9
Y1 - 2013/9
N2 - Extracellular signal-regulated kinase (ERK) is known to be phosphorylated after exposure to noxious stimuli. In this study, we investigated the response in the dura mater to nociceptive stimulation, which is thought to be responsible for the pathogenesis of headaches, including migraines. We also examined the level of ERK phosphorylation in the trigeminal ganglion following cortical spreading depression (CSD), which is thought to play an important role in migraine pathophysiology. Western blot and immunohistochemical analyses showed a significant increase in the ERK phosphorylation levels 3. min following an application of 10. mM capsaicin to the dura mater. This increase was inhibited after an application of the TRPV1 antagonist capsazepine or a MEK inhibitor. An immunohistochemical analysis revealed that most of the small-sized trigeminal ganglion neurons with TRPV1-immunoreactivity that innervate the dura mater exhibited pERK-immunoreactivity, suggesting that these neurons had responded to nociceptive stimulation. CSD increased the level of ERK phosphorylation 30. min after its elicitation, and this response was inhibited by a prior intraventricular administration of TRPV1 antagonist. These results indicate that CSD can activate dural TRPV1 to send nociceptive signals to the trigeminal system, and they provide important clues regarding the relationship between CSD and the trigeminovascular system.
AB - Extracellular signal-regulated kinase (ERK) is known to be phosphorylated after exposure to noxious stimuli. In this study, we investigated the response in the dura mater to nociceptive stimulation, which is thought to be responsible for the pathogenesis of headaches, including migraines. We also examined the level of ERK phosphorylation in the trigeminal ganglion following cortical spreading depression (CSD), which is thought to play an important role in migraine pathophysiology. Western blot and immunohistochemical analyses showed a significant increase in the ERK phosphorylation levels 3. min following an application of 10. mM capsaicin to the dura mater. This increase was inhibited after an application of the TRPV1 antagonist capsazepine or a MEK inhibitor. An immunohistochemical analysis revealed that most of the small-sized trigeminal ganglion neurons with TRPV1-immunoreactivity that innervate the dura mater exhibited pERK-immunoreactivity, suggesting that these neurons had responded to nociceptive stimulation. CSD increased the level of ERK phosphorylation 30. min after its elicitation, and this response was inhibited by a prior intraventricular administration of TRPV1 antagonist. These results indicate that CSD can activate dural TRPV1 to send nociceptive signals to the trigeminal system, and they provide important clues regarding the relationship between CSD and the trigeminovascular system.
KW - Cortical spreading depression
KW - ERK
KW - Trigeminal ganglion
KW - TRPV1
UR - http://www.scopus.com/inward/record.url?scp=84886397504&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84886397504&partnerID=8YFLogxK
U2 - 10.1016/j.neures.2013.08.001
DO - 10.1016/j.neures.2013.08.001
M3 - Article
C2 - 23962823
AN - SCOPUS:84886397504
VL - 77
SP - 110
EP - 119
JO - Neuroscience Research
JF - Neuroscience Research
SN - 0168-0102
IS - 1-2
ER -