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What does GIRK stand for?

GIRK stands for G-protein-regulated, inwardly rectifying K

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The spectrum of action of flupirtine includes analgesia, muscle relaxation, and neuroprotection. The analgesic effect of flupirtine does not appear to be associated with any central opioid effect. Flupirtine does not appear to act on the usual binding sites of the N-methyl-D-aspartate receptor (NMDA) such as glycine site or polyamine site or the magnesium site. There is evidence to show that flupirtine may suppress the opening of the NMDA channel by acting as an oxidizing agent at the redox site of the NMDA receptor. Jakob and Krieglstein found an activation of G protein-regulated inwardly rectifying.
The above descriptions ignore the effects of Gß?–signalling, which can also be important, in particular in the case of activated Gai/o-coupled GPCRs. The primary effectors of Gß? are various ion channels, such as G-protein-regulated inwardly rectifying.
The above descriptions ignore the effects of Gß?–signalling, which can also be important, in particular in the case of activated Gai/o-coupled GPCRs. The primary effectors of Gß? are various ion channels, such as G-protein-regulated inwardly rectifying.
Flupirtin greift als zentral wirksames Analgetikum an der postsynaptischen Membran an. Es wirkt nicht über eine Beeinflussung der Glutamat-Ausschüttung/Übertragung wie die Opioide, sondern öffnet selektiv einwärtsgerichtete Kaliumkanäle („GIRK“, G-Protein regulated inwardly rectifying K+ channels) an der postsynaptischen Membran. [1] Dadurch stabilisiert sich das Ruhemembranpotential, so dass die Schmerzweiterleitung gehemmt ist.