Stimulering af N. Vagus (GIRK's)

Kan se du har teksten fra Boron + Boulpeap... Vil tro det er en fejl og at der skal stå outward i stedet, hvilket vil give meget mere mening... Virker usandsynligt at K frivillig skulle diffundere mod så stor koncentrationsforskel og at det samtidig skulle have modsat effekt af hvad man ville tro... Så GIRK kanalerne må åbne for en indadgående strøm...

... Men inward opræder rigtig nok i navnet så synes det er mærkeligt...

Hej stensalt.

Jeg tænkte også selv at det måtte være en fejl, men wiki skrev det samme, så blev i tvivl. Har dog fundet ud af at vedkommende som har skrevet på wiki har fejlciteret artiklen han linker til, og at det også var en fejl i bogen (fandt to andre steder i bogen som skrev præcist det samme bortset fra ordet inward er skiftet med outward)

Disse GIRKS er også i stand til at lede K ind af cellen, omend i mindre grad en ud -> self. afhængigt af membranpotentiale, og ligevægtspotentialet for K.

Ergo cellen hyperpolariseres pga. en udadgående kalium strøm.

MVH

Hej stensalt.

Tak for svaret.

Har efter yderligere læsning fundet ud af det. Jeg mente selv det måtte være en fejl i bogen, men da jeg tjekkede wiki skrev den det samme: 

Examples of GIRKs include a subset of potassium channels in the heart which when activated by parasympathetic signals such as acetylcholine through M2 muscarinic receptors, causes an inward current of potassium which slows down the heart rate.[3][4] These are called muscarinic potassium channels (IKACh) and are heterotetramers comprised of two GIRK1 and two GIRK4 subunits.[5][ (http://en.wikipedia.org/wiki/G_protein-coupled_inwardly-rectifying_potassium_channel).

Jeg tror dog forfatteren til på wiki har fået den artikel han citerer galt i halsen:

Inward rectifier K+ channels ... help set the resting potential of a cell near the K+ equilibrium potential (EK) by conducting substantial inward K+ currents at membrane potentials negative to EK and small outward currents at voltages positive to EK

og

IRK regulation by an intracellular pathway involves the hormonal stimulation of a cardiac K+ current termed lKACh (Hille, 1992). Following
acetylcholine release from the vagus nerve, m2 muscarinic acetylcholine receptors (mAChRs) expressed on atrial cells activate heterotrimeric (af3y) guanine nucleotide- binding (G) proteins that in turn stimulate the IK~c,, channel (Soejima and Noma, 1984; Pfaffinger et al., 1985; Breitweiser and Szabo, 1985). The increased K+ conductance
due to lKACh reduces the rate at which cardiac pacemaker cells depolarize and thus slows heart contraction.

http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6WSN-4C59G1Y-14-1&_cdi=7051&_user=10&_orig=search&_coverDate=11%2F03%2F1995&_sk=999169996&view=c&wchp=dGLbVlW-zSkzk&md5=4cba455b9ab039577b7a5ab7404683b1&ie=/sdarticle.pdf

Yderligere fandt jeg i min fysiologibog (Boron & Boulpaep) følgende:

G PROTEIN-ACTIVATED K+ CURRENT.
Body_ID: HC020010
Acetylcholine activates muscarinic receptors and, through the βγ subunits of a G protein, activates an outward K+ current mediated by GIRK K+ channels (see p. 197). This current is prominent in SA and AV nodal cells, where it decreases pacemaker rate when activated by cell hyperpolarization. It also slows the conduction of the action potential through the AV node.

samt, dette billede vedhæftet (håber jeg?), og billedtekst:

Ionotropic and meta-botropic acetylcholine receptors. A, This example illustrates a "nicotinic" acetylcholine receptor, which is a ligand-gated channel on the postsynaptic membrane. In a skeletal muscle, the end result is muscle contraction. B, This example illustrates a "muscarinic" acetylcholine receptor, which is coupled to a heterotrimeric G protein. In a cardiac muscle, the end result is decreased heart rate. Note that the presynaptic release of ACh is very similar here and in A. ACh, acetylcholine; GTP, guanosine triphosphate.