What is the importance of Nernst Equilibrium Potential practically? Especially when you do patch clamp experiments?
Hi,
The Nernst equation for a given ion determines the difference of potential at both sides of the membrane at which this ion is at equilibrium between inward and outward flux (zero net current). This is important for different things:
First, we can take advantage to bring the cell (including neurons) to a given potential for setting a zero current for an ion, which allows us to better observe other currents. This is typically happening when we want to observe in a patched neuron the synaptic input of Na+ (excitatory currents mediated by glutamate receptors) or Cl- and K+ (inhibitory currents mediated by GABA receptors).
In adition, the equilibrium potential for a group of ions in a membrane gives us a measure of how is this membrane at rest, so we can draw a baseline to measure how is its function or behavior in a given state which is not at rest. This is why we call sometimes the equilibrium potential of a group of ions in a membrane as 'resting potential', that as Wikipedia says, is 'relatively static'. Maybe it is better 'relatively dynamic', as there are some small ionic currents that in average drive the potential at rest. We say that in the resting state the cell is not excited, in contrast of incoming membrane fuctuations such as subtreshold synaptic activity or action potentials.
Hope that helped!
The difference (V(t)-V_e) is the force that drives ions through the membrane channels when they open. Of course here V_e is the Nernst equilibrium potential for a given ion. So, for the Ohm's law the current for a given ion type will be given as : I(t)=g_ion(V(t)-V_ion)), with g_ion being the conductance of that ion (i.e. the inverse of the resistance). So to know the equilibrium potential of a ionic type permit to estimate the current for that ion once the conductance is known.
Hi, as the Nernst potential gives the membrane voltage at which a given ion is at its equilibrium concerning diffusion across the membrane (no net ion flux), you can predict the direction the ion current or flux at a given membrane voltage that has been measured or clamped. In practice, 100 mM K+ inside the cell and 1 mM K+ outside gives a Nernst equilibrium potential of -118 mV. If you measure a membrane voltage of - 70 mV, you can expect an efflux of K+ by (facilitated) diffusion, e.g. through open ion channels
Hi, this equation basically gives an indication of the direction and magnitude of change in potential across the membranes in excitable cells upon stimulation.It takes into account the change in conductance of a single ion. It cannot predict the potential during resting status as it only takes into account the concentration of a single ion.
When you set your membrane potential to the equilibrium potential of a specific ion, its curren will be null. Meaning that without pharmacology you can record IPSC if you set your holding potential to 0 mV (reverse potential of EPSC), and vice versa, you can record EPSC when you set your holding potential to Ecl.
As Gerhard simplified, the diffusion of (let say potassium) ions across the membrane can be predicted and K-ion current (or flux) can be calculated (and measured in patch clamp study to compare with calculations) at any given membrane voltage. From Gerhard example (100 mM K+ inside the cell and 1 mM K+ outside gives a Nernstian equilibrium potential of about -118 mV) the difference between resting cell membrane potential, Em (about - 70 mV), and Nernst potential will be ~50 mV to produce K-diffusion (K-efflux). Therefore, the cell is loosing potassium constantly if K-channels are open (Kir, 2P domain pore, Kv, Ka, Kd channels). So, practically in life, Na-K-pump should always return potassium back into the cell. When we do patch clamp study we use holding potential (simply to substitute Na-K-pump) and keep a cell close to the resting Em before voltage-step or voltage-ramp protocol applied for current stimulation/study.
Interestingly, even glial cells (astrocytes, NG-2, oligodenrocytes, Muller or Bergmann glia, etc) have a definition to be like "K-electrodes", their resting membrane potentials (~-90 mV) are still always more positive than their Nernst potential (~ -120 mV) and thus these cells (i) are far from to be an ideal K-electrode, (ii) have always some leakage (sodium, potassium for example) and (iii) the cells should have essential Na-K-pump to keep proper K concentration inside and highly hyperpolarized Em; otherwise the cells will lose the function.
Practically, what is bad if we clamp a cell at higher or lower potential than their Em? We then strongly affect internal ion composition and channel study became insufficient.