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Dural administration of inflammatory soup or Complete Freund's Adjuvant induces activation and inflammatory response in the rat trigeminal ganglion.

Lukács M, Haanes KA, Majláth Z, Tajti J, Vécsei L, Warfvinge K, Edvinsson L - J Headache Pain (2015)

Bottom Line: We hypothesize that migraine pain originates from a central mechanism that results secondarily in hypersensitivity in peripheral afferents associated with the cerebral and cranial blood vessels.Myography resulted in a strong vasoconstrictor response to IS, but not to CFA.These results suggest that the application of IS or CFA onto the dura mater causes long-term activation of the TG and demonstrate the importance of the neuro-glial interaction in the activation of the trigeminovascular system.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Institute of Clinical Sciences, Division of Experimental Vascular Research, Lund University, Sölvegatan 17, SE 221 84, Lund, Sweden.

ABSTRACT

Background: Migraine is a painful disorder with a huge impact on individual and public health. We hypothesize that migraine pain originates from a central mechanism that results secondarily in hypersensitivity in peripheral afferents associated with the cerebral and cranial blood vessels. It has previously been shown that application of inflammatory or algesic substances onto the dura mater or chemical stimulation of the dural receptive fields causes hypersensitivity to mechanical and thermal stimulation together with direct activation of the TG. We asked whether local inflammation of dura mater induces inflammatory activation in the trigeminal ganglion.

Methods: We performed topical administration of inflammatory soup (IS) or Complete Freund's Adjuvant (CFA) onto an exposed area of the rat dura mater in vivo for 20 min. The window was closed and the rats were sacrificed after 4 h and up to 7 days. Myography was performed on middle meningeal arteries. The trigeminal ganglia were removed and processed for immunohistochemistry or Western blot.

Results: Both CFA and IS induced enhanced expression of pERK1/2, IL-1β and CGRP in the trigeminal ganglia. The pERK1/2 immunoreactivity was mainly seen in the satellite glial cells, while IL-1β reactivity was observed in the neuronal cytoplasm, close to the cell membrane, seemingly as sign of neuro-glial interaction. The CGRP expression in the neurons and nerve fibres was enhanced after the application of either inflammatory agent. Myography resulted in a strong vasoconstrictor response to IS, but not to CFA.

Conclusions: These results suggest that the application of IS or CFA onto the dura mater causes long-term activation of the TG and demonstrate the importance of the neuro-glial interaction in the activation of the trigeminovascular system.

No MeSH data available.


Related in: MedlinePlus

Myograph recordings on middle menigeal arteries. a IS caused a vasocontraction of the middle menigeal artery. b CFA did not show any significant changes in vasocontractility (n = 5)
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Fig7: Myograph recordings on middle menigeal arteries. a IS caused a vasocontraction of the middle menigeal artery. b CFA did not show any significant changes in vasocontractility (n = 5)

Mentions: In our model, we observe activation of the trigeminal ganglion using the inflammatory substances CFA and IS. Based on the vascular theory of migraine, we wanted to see if the agents caused vasodilation or vasocontraction when applied to the middle meningeal artery. MMAs from fresh rats were isolated and mounted in a wire myograph. IS caused a strong contraction of the MMAs (Fig. 7a), whereas CFA did not result in any vasomotor response (Fig. 7b). It is worth mentioning that CFA consists largely of mineral oil and is not water soluble. No vasomotor effects occurred when CFA was added directly onto the MMA in the myograph (data not shown).Fig. 7


Dural administration of inflammatory soup or Complete Freund's Adjuvant induces activation and inflammatory response in the rat trigeminal ganglion.

Lukács M, Haanes KA, Majláth Z, Tajti J, Vécsei L, Warfvinge K, Edvinsson L - J Headache Pain (2015)

Myograph recordings on middle menigeal arteries. a IS caused a vasocontraction of the middle menigeal artery. b CFA did not show any significant changes in vasocontractility (n = 5)
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556720&req=5

Fig7: Myograph recordings on middle menigeal arteries. a IS caused a vasocontraction of the middle menigeal artery. b CFA did not show any significant changes in vasocontractility (n = 5)
Mentions: In our model, we observe activation of the trigeminal ganglion using the inflammatory substances CFA and IS. Based on the vascular theory of migraine, we wanted to see if the agents caused vasodilation or vasocontraction when applied to the middle meningeal artery. MMAs from fresh rats were isolated and mounted in a wire myograph. IS caused a strong contraction of the MMAs (Fig. 7a), whereas CFA did not result in any vasomotor response (Fig. 7b). It is worth mentioning that CFA consists largely of mineral oil and is not water soluble. No vasomotor effects occurred when CFA was added directly onto the MMA in the myograph (data not shown).Fig. 7

Bottom Line: We hypothesize that migraine pain originates from a central mechanism that results secondarily in hypersensitivity in peripheral afferents associated with the cerebral and cranial blood vessels.Myography resulted in a strong vasoconstrictor response to IS, but not to CFA.These results suggest that the application of IS or CFA onto the dura mater causes long-term activation of the TG and demonstrate the importance of the neuro-glial interaction in the activation of the trigeminovascular system.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine, Institute of Clinical Sciences, Division of Experimental Vascular Research, Lund University, Sölvegatan 17, SE 221 84, Lund, Sweden.

ABSTRACT

Background: Migraine is a painful disorder with a huge impact on individual and public health. We hypothesize that migraine pain originates from a central mechanism that results secondarily in hypersensitivity in peripheral afferents associated with the cerebral and cranial blood vessels. It has previously been shown that application of inflammatory or algesic substances onto the dura mater or chemical stimulation of the dural receptive fields causes hypersensitivity to mechanical and thermal stimulation together with direct activation of the TG. We asked whether local inflammation of dura mater induces inflammatory activation in the trigeminal ganglion.

Methods: We performed topical administration of inflammatory soup (IS) or Complete Freund's Adjuvant (CFA) onto an exposed area of the rat dura mater in vivo for 20 min. The window was closed and the rats were sacrificed after 4 h and up to 7 days. Myography was performed on middle meningeal arteries. The trigeminal ganglia were removed and processed for immunohistochemistry or Western blot.

Results: Both CFA and IS induced enhanced expression of pERK1/2, IL-1β and CGRP in the trigeminal ganglia. The pERK1/2 immunoreactivity was mainly seen in the satellite glial cells, while IL-1β reactivity was observed in the neuronal cytoplasm, close to the cell membrane, seemingly as sign of neuro-glial interaction. The CGRP expression in the neurons and nerve fibres was enhanced after the application of either inflammatory agent. Myography resulted in a strong vasoconstrictor response to IS, but not to CFA.

Conclusions: These results suggest that the application of IS or CFA onto the dura mater causes long-term activation of the TG and demonstrate the importance of the neuro-glial interaction in the activation of the trigeminovascular system.

No MeSH data available.


Related in: MedlinePlus