The resting membrane potential is primarily established by the Na⁺/K⁺ pump and the selective permeability of the membrane to ions, particularly K⁺. The Na⁺/K⁺ pump actively transports three Na⁺ ions out of the cell and two K⁺ ions into the cell, contributing to a negative charge inside the cell. The Donnan effect, which describes the distribution of ions across a membrane due to the presence of impermeant solutes, plays a role in influencing ion concentrations but is not the primary determinant of resting membrane potential. Thus, while both mechanisms are involved in cellular ion balance, the Na⁺/K⁺ pump is the key player in setting the resting membrane potential.
Increasing the extracellular potassium concentration can depolarize the resting membrane potential, making it less negative. This can lead to increased excitability of the cell.
The Donnan effect refers to the uneven distribution of ions across a semipermeable membrane, affecting osmotic pressure by causing water to move across the membrane. In capillaries, this can impact fluid balance between blood and tissues. The Donnan effect can also influence pH by affecting the distribution of charged molecules, such as ions or proteins, leading to changes in the local pH levels.
Hypokalemia (low potassium levels) can lead to a more negative resting membrane potential in cells. This enhances the threshold for depolarization and can result in muscle weakness, cramping, and cardiac arrhythmias due to impaired cell signaling.
During depolarization, sodium (Na) rushes into the neuron through Na channels (at the Nodes of Ranvier between the bundles of myelin "insulation"). Less Na in the extracellular fluid would mean there would be less to rush in. So, the neuron would not be depolarized as well. The resting membrane potential would be more positive on the inside.
Resting membrane potential is determined by K+ concentration gradient and cell's resting permeability to K+, N+, and Cl-.Gated channels control ion permeability. Three types of gated channels are mechanically gated, chemical gated, voltage gated. Threshold voltage varies from one channel type to another.The Goldmann- Hodgkins-Katz Equation predicts membrane potential using multiple ionsThe resting potentialBecause the plasma membrane is highly permeable to potassium ions, the resting potential is fairly close to -90mV, the equilibrium potential for K+Although the electrochemical gradient for sodium ions is very large, the membrane's permeability to these ions is very low. Consequently, Na+ has only a small effect on the normal resting potential, making it just slightly less negative than it would be otherwise.The sodium-potassium exchange pump ejects 3 Na+ ions for every 2 K+ ions that it brings into the cell. It thus serves to stabilize the resting potential when the ratio of Na+ entry to K+ loss through passive channels is 3:2.At the normal resting potential, these passive and active mechanisms are in balance. The resting potential varies widely with the type of cell. A typical neuron has a resting potential of approx -70mV
Ouabain blocks the Na+/K+ ATPase pump, preventing it from properly maintaining the Na+ and K+ gradients across the cell membrane. This disrupts the resting membrane potential and impairs the neuron's ability to generate action potentials.
The Donnan equilibrium effect can be correlated to living cells. Cell membranes are selectively permeable, which means that they allow some molecules to pass through while keeping others out.The flow of molecules and ions between a cell and its environment is regulated by the Donnan effect. Living cells contain impermeable anionic colloids, which are mostly made up of proteins and organic phosphates; and these colloidal anions cannot cross the cell membrane.As a result of this, there is a high concentration of non-diffusible anions across the cell membrane, thus creating the Donnan Equilibrium. This means that there are more ions inside the cell than outside. For ease of explanation let's call this Donnan Equilibrium 1.What does this do to cells? Water will continuously move into the cell by the process of osmosis. If this process continues, the cells will inevitably rupture.What is the mechanism that prevents cells from swelling and rupturing?The answer is the sodium pump (Na⁺- K⁺ ATPase) in the cell membrane. It is the most ubiquitous system in animal cells. The presence of the ATP-driven Na⁺ and K⁺ pump is nature's way of preventing cells from rupturing by continuously pushing out excess ions. The pump together with the membrane's low permeability to sodium effectively prevents sodium from entering the cell. The sodium pump renders the membrane impermeable to sodium, setting up a second Donnan Equilibrium (let's call this Donnan Equilibrium 2).The earlier Donnan effect (Donnan Equilibrium 1) with respect to impermeable anionic colloids balances the latter Donnan effect (Donnan Equilibrium 2) of impermeable extracellular sodium. The balancing act between these two effects is by way of allowing cells to maintain and regulate normal cell volume in living functions.Hope this answers the question.
No, neurotransmitters that depress the resting potential are called inhibitory neurotransmitters. Excitatory neurotransmitters have the opposite effect, causing depolarization and increasing the likelihood of an action potential.
Hyperkalemia is an increase in extracellular K. Driving force of an ion depends on two factors, voltage and concentration gradient. For K voltage gradient is pushing K into the cell but the concentration gradient is driving K out of the cell. However, the total driving force for K is out of the cell because the concentration gradient is that strong. When there is an increase in K on the outside, the driving force for K decreases.The equilibrium potential for K is -95mV. This means if K was freely permeable to the cell's membrane, it would reach equilibrium at -95mV. Another way to look at this is that efflux of K is the same as influx of K and the cell's new resting membrane potential would increase from a normal value of -70mV to -95mV. Note that I said it would increase even though the value became more negative. This is because the change in membrane potential has increased.Since the driving force of K has decreased, the equilibrium potential has also decreased. From a value of -95mV it is decreased to let's just say -80mV. Since a normal resting membrane potential is regularly -70mV, the decrease in equilibrium potential of K has decreased this resting membrane potential to say -60mV now. This is a depolarization of the cell.If this process happens quickly, it will depolarize the cell to the threshold value and you will have an action potential. However, if the hyperkalemia is severe, the cell will stay depolarized because the K equilibrium has decreased to a point where the cell cannot hyperpolarize back to threshold or resting membrane potential.If this process happens slowly, the inactivation gates of the sodium voltage-gated channels will automatically shut and the cell cannot depolarize even if it reaches threshold values. It must hyperpolarize back to resting membrane potential and the inactivation gates of the sodium voltage-gated channel will reopen.
Doubling the number of Na leakage channels in the plasma membrane would result in an increased passive influx of sodium ions into the cell. This could disrupt the ion balance and potentially lead to changes in membrane potential and cell function.
Opening of potassium channels allows potassium ions to move out of the neuron, leading to hyperpolarization by increasing the negative charge inside the neuron. This action increases the charge difference across the membrane, known as the resting membrane potential, making the neuron less likely to fire an action potential.
The resting membrane potential is maintained by the distribution of positive and negative charged ions across both sides of the cell membrane. At rest, calcium concentration in cells of the heart is low as compared to the outside. At action, calcium channels in the membranes open, thereby allowing calcium to rush into the cells. So raising the heart rate.