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[Gap junctional intercellular communication: a new mechanism in pathophysiology of migraine with aura. Therapeutic applications].
Pathol Biol (Paris) 2012; 60(6):392-8PB

Abstract

Migraine is a common, recurrent and disabling primary headache disorder, which affects up to 20% of the population. About a third of patients with migraine have attacks with aura, a focal neurological disturbance that manifests itself as visual, sensitive or motor symptoms. Cortical spreading depression, a wave of electrical activity that moves across the cerebral cortex through neuronal-glial cell gap junctions, would be involved in the triggering of migraine aura. Moreover, cortical spreading depression activates perivascular trigeminal afferents in the neocortex, that through central and peripheral reflex, cause inflammatory reaction in the meninges to generate the headache. Tonabersat, a novel benzopyran compound, was selected for clinical trial on the basis of its inhibitory activity on cortical spreading depression and neurogenic inflammation in animal models of migraine. Moreover, tonabersat inhibited trigeminal ganglion neuronal-glial cell gap junctions, suggesting that this compound could prevent peripheral sensitization within the ganglion. In clinical trial, tonabersat showed a preventive effect on attacks of migraine with aura but had no efficacy on non-aura attacks and in the acute treatment of migraine. In conclusion, neuronal-glial cell gap junctional intercellular communication seems to be involved in the pathophysiology of migraine with aura and is emerging as a new promising therapeutic target for prophylactic treatment of patients with chronic attacks.

Authors+Show Affiliations

Institut de physiologie et de biologie cellulaire, FRE CNRS 3511, université de Poitiers, 40 avenue du Recteur-Pineau, Poitiers cedex, France. Denis.Sarrouilhe@univ-poitiers.frNo affiliation info available

Pub Type(s)

English Abstract
Journal Article
Review

Language

fre

PubMed ID

22633071

Citation

Sarrouilhe, D, and C Dejean. "[Gap Junctional Intercellular Communication: a New Mechanism in Pathophysiology of Migraine With Aura. Therapeutic Applications]." Pathologie-biologie, vol. 60, no. 6, 2012, pp. 392-8.
Sarrouilhe D, Dejean C. [Gap junctional intercellular communication: a new mechanism in pathophysiology of migraine with aura. Therapeutic applications]. Pathol Biol. 2012;60(6):392-8.
Sarrouilhe, D., & Dejean, C. (2012). [Gap junctional intercellular communication: a new mechanism in pathophysiology of migraine with aura. Therapeutic applications]. Pathologie-biologie, 60(6), pp. 392-8. doi:10.1016/j.patbio.2012.04.002.
Sarrouilhe D, Dejean C. [Gap Junctional Intercellular Communication: a New Mechanism in Pathophysiology of Migraine With Aura. Therapeutic Applications]. Pathol Biol. 2012;60(6):392-8. PubMed PMID: 22633071.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Gap junctional intercellular communication: a new mechanism in pathophysiology of migraine with aura. Therapeutic applications]. AU - Sarrouilhe,D, AU - Dejean,C, Y1 - 2012/05/25/ PY - 2012/03/19/received PY - 2012/04/12/accepted PY - 2012/5/29/entrez PY - 2012/5/29/pubmed PY - 2013/5/31/medline SP - 392 EP - 8 JF - Pathologie-biologie JO - Pathol. Biol. VL - 60 IS - 6 N2 - Migraine is a common, recurrent and disabling primary headache disorder, which affects up to 20% of the population. About a third of patients with migraine have attacks with aura, a focal neurological disturbance that manifests itself as visual, sensitive or motor symptoms. Cortical spreading depression, a wave of electrical activity that moves across the cerebral cortex through neuronal-glial cell gap junctions, would be involved in the triggering of migraine aura. Moreover, cortical spreading depression activates perivascular trigeminal afferents in the neocortex, that through central and peripheral reflex, cause inflammatory reaction in the meninges to generate the headache. Tonabersat, a novel benzopyran compound, was selected for clinical trial on the basis of its inhibitory activity on cortical spreading depression and neurogenic inflammation in animal models of migraine. Moreover, tonabersat inhibited trigeminal ganglion neuronal-glial cell gap junctions, suggesting that this compound could prevent peripheral sensitization within the ganglion. In clinical trial, tonabersat showed a preventive effect on attacks of migraine with aura but had no efficacy on non-aura attacks and in the acute treatment of migraine. In conclusion, neuronal-glial cell gap junctional intercellular communication seems to be involved in the pathophysiology of migraine with aura and is emerging as a new promising therapeutic target for prophylactic treatment of patients with chronic attacks. SN - 1768-3114 UR - https://www.unboundmedicine.com/medline/citation/22633071/[Gap_junctional_intercellular_communication:_a_new_mechanism_in_pathophysiology_of_migraine_with_aura__Therapeutic_applications]_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0369-8114(12)00049-1 DB - PRIME DP - Unbound Medicine ER -