Clinical connexions

Alldredge, B

doi:10.1136/jcp.2008.055699

Cited by 14 publications

(12 citation statements)

References 132 publications

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“…The propagation of hypoxic injury depletes GABAergic interneurons Ca 2þ buffering-capacity and affects GABA-transmission (Nitsch et al, 1989;Schwartz-Bloom and Sah, 2001;Frantseva et al, 2002;Thompson et al, 2006;Zhan et al, 2006;Alldredge, 2008;Uteshev, 2012). In this condition, α7nAChRs and Cx36-channels can mediate toxic Ca 2þ overloads and pathologic interneuronal transients.…”

Section: Discussionmentioning

confidence: 99%

Hippocampal GABAergic interneurons coexpressing alpha7-nicotinic receptors and connexin-36 are able to improve neuronal viability under oxygen–glucose deprivation

Voytenko¹,

Lushnikova²,

Savotchenko³

et al. 2015

Brain Research

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Section: Discussionmentioning

confidence: 99%

Hippocampal GABAergic interneurons coexpressing alpha7-nicotinic receptors and connexin-36 are able to improve neuronal viability under oxygen–glucose deprivation

Voytenko¹,

Lushnikova²,

Savotchenko³

et al. 2015

Brain Research

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“…Changes in Cx expression and GJIC capacity were described in brain injuries and dysfunctions as inflammation, epilepsy, and neurodegenerative diseases (Rouach et al, 2002). Thereby, gap junction channels have progressively appeared as potential therapeutic targets in the treatment of a growing number of CNS diseases (Alldredge, 2008). …”

Section: Gap Junction Channels and Hemichannels In The Central Nervoumentioning

confidence: 99%

Involvement of gap junction channels in the pathophysiology of migraine with aura

Sarrouilhe¹,

Dejean²,

Mesnil³

2014

Front. Physiol.

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Migraine is a common, recurrent, and disabling primary headache disorder with a genetic component which affects up to 20% of the population. One third of all patients with migraine experiences aura, a focal neurological disturbance that manifests itself as visual, sensitive or motor symptoms preceding the headache. In the pathophysiology of migraine with aura, activation of the trigeminovascular system from the meningeal vessels mediates migraine pain via the brainstem and projections ascend to the thalamus and cortex. Cortical spreading depression (CSD) was proposed to trigger migraine aura and to activate perivascular trigeminal nerves in the cortex. Quinine, quinidine and the derivative mefloquine are able to inhibit CSD suggesting an involvement of neuronal connexin36 channels in CSD propagation. More recently, CSD was shown to induce headache by activating the trigeminovascular system through the opening of stressed neuronal Pannexin1 channels. A novel benzopyran compound, tonabersat, was selected for clinical trial on the basis of its inhibitory activity on CSD and neurogenic inflammation in animal models of migraine. Interestingly, in the time course of animal model trials, tonabersat was shown to inhibit trigeminal ganglion (TGG) neuronal-glial cell gap junctions, suggesting that this compound could prevent peripheral sensitization within the ganglion. Three clinical trials aimed at investigating the effectiveness of tonabersat as a preventive drug were negative, and conflicting results were obtained in other trials concerning its ability to relieve attacks. In contrast, in another clinical trial, tonabersat showed a preventive effect on attacks of migraine with aura but had no efficacy on non-aura attacks. Gap junction channels seem to be involved in several ways in the pathophysiology of migraine with aura and emerge as a new promising putative target in treatment of this disorder.

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“…In vertebrates, gap junctions are composed of members of a closely related family of four-transmembrane–containing proteins known as connexins. Mutations in connexins are responsible for at least 10 human diseases, underscoring the essential role of these proteins in tissue development and homeostasis (Alldredge, 2008). …”

Section: Introductionmentioning

confidence: 99%