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The cell membrane potential created by potassium and sodium ions allows the cell to generate an action potential a "spike" of electrical discharge.
The positive lysosomal membrane potential, created by the influx of protons, reciprocally, could prevent the V-ATPase from continuing to pump protons.
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This quantal release of neurotransmitter has a critical influence on the electrical potential created in the postsynaptic membrane.
This dramatically lowers the membrane potential and creates an environment for electrochemical oxidation of Ru.
They can be used to examine fluxes in mitochondrial membrane potential, or create dynamic coculture environments where individual subpopulations can be identified.
This hyperpolarization activates the HCN channels and allows an inward current, depolarizing it in the direction of the resting membrane potential and thus creating a sag in the voltage.
Instead, sodium ions are expelled and potassium ions taken up by the Na⁺/K⁺-ATPase, potassium ions then flow down their concentration gradient through potassium-selection ion channels, this loss of positive charge creates a negative membrane potential.
This sudden increase in cardiac membrane potential is transmitted from cell to cell, creating a wave of depolarization that functionally represents the excitation signal of the heart.
This kit included the mitochondrial membrane potential disrupter, CCCP, which was used to create loss of MOMP in ookinetes.
Electrons are exchanged down the chain at increasing reduction potentials from complexes I through IV, allowing the shuttling of protons across the mitochondrial membrane creating a proton gradient (membrane potential).
The resting membrane potential is largely maintained via an adenosine triphosphate (ATP) driven primary active 3Na+/2K+ exchange pump creating both chemical and electric gradients across the cellular membrane and via a passive K+ outward flux.
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