Membrane potential is the imbalance of charges across the cell membrane; inside the cell is negative and outside is positive, creating a potential difference.
This potential arises from ionic concentration differences between the intracellular fluid (ICF) and extracellular fluid (ECF) and the selective permeability of the membrane.
Ion gradients are maintained by transport mechanisms; some ions have leaky channels that allow passive movement, creating leakage that affects the potential.
Potassium (K⁺) tends to be higher inside the cell; passive movement through leak channels allows K⁺ to leave the cell along its concentration gradient, contributing to a negative interior.
Sodium (Na⁺) is higher outside; sodium movement into the cell also affects the potential, especially during action potentials when channels open.
The kidney’s handling of potassium excretion is important because cellular function across many cell types depends on potassium balance, which is tied to the overall membrane potential.
The resting membrane potential (RMP) is around -70 mV in many cells, but can vary; it is influenced by ion gradients and leak conductances.
Equilibrium potentials (e.g., for K⁺ and Na⁺) define the membrane potential that would exist if only one ion type determined the potential.
There is reference to an equilibrium potential of potassium and to how the system would behave if K⁺ could pass freely across the membrane; the outward flow of K⁺ drives the interior toward more negative values.
The overall homeostasis of ions and potential is essential for cellular excitability, signaling, and function.
Action Potential and Resting Potential
An action potential is a rapid change in membrane potential, moving from a resting state toward a positive peak and then returning to rest.
Resting membrane potential (RMP) is approximately V_m \,\approx -70\ \text{mV} (as discussed in the lecture).
The membrane has a threshold around V_m \approx -50\ \text{mV}; if the depolarization reaches this threshold, an action potential is triggered.
Depolarization: membrane potential rises from rest toward a positive value; during an action potential, it peaks around V_m \approx +40\ \text{to}\ +50\ \text{mV} (the lecture notes mention around +40 to +50 mV).
The peak of the action potential is the result of rapid opening of voltage-gated Na⁺ channels, allowing a large inward Na⁺ current.
The peak Na⁺ current is consistent with the equilibrium potential of Na⁺, which is approximately E_{Na} \approx +30\ \text{to}\ +40\ \text{mV}, as suggested by the Nernst principle.
The Na⁺/K⁺ ATPase pump and non-voltage-gated channels contribute to maintaining the resting gradient; the pump is a carrier that maintains ion concentration differences and thus supports the resting potential, separate from the voltage-dependent channels that open during an action potential.
The depolarization phase is not driven by a single channel opening but by many channels opening synchronously; thousands of channels contribute to the rapid upstroke.
Repolarization follows the peak as voltage-gated K⁺ channels open, allowing K⁺ to exit the cell and bring the membrane potential back toward the resting value.
Hyperpolarization occurs when the membrane potential temporarily becomes more negative than the RMP, before it returns to baseline (RMP).
An action potential is considered a rapid change in membrane potential that enables cell signaling and rapid responses (e.g., muscle contraction, neural signaling).
The lecture emphasizes that the resting potential and the action potential are influenced by the balance of pumps (like Na⁺/K⁺ ATPase) and channels (which are not voltage-gated for setting RMP, but voltage-gated for the action potential).
Nernst Equilibrium Potentials and Ion Considerations
Equilibrium potential for an ion (e.g., K⁺, Na⁺) is the membrane potential that would exist if only that ion determined the membrane potential.
Nernst equation is used to calculate equilibrium potentials:
For Na⁺, the equilibrium potential is typically around E_{Na} \approx +30\ \text{to}\ +40\ \text{mV}, aligning with the observed peak depolarization values.
The balance of these potentials and the conductances of the membrane give the overall membrane potential during resting and active states.
Synapses, EPSP, and IPSP
The basic signaling across a synapse involves a presynaptic neuron and a postsynaptic cell (which can be another neuron or a muscle cell).
The synaptic cleft is the small gap between the presynaptic terminal and the postsynaptic cell where neurotransmitters are released.
An action potential in the nerve (presynaptic) triggers neurotransmitter release into the synaptic cleft; receptors on the postsynaptic cell respond to these neurotransmitters.
If the postsynaptic response is excitatory, it is called an EPSP (excitatory postsynaptic potential), typically due to Na⁺ influx that makes the inside more positive (depolarization).
The EPSP makes it easier to reach threshold and fire an action potential in the postsynaptic cell.
If the response is inhibitory, it is called an IPSP (inhibitory postsynaptic potential), which hyperpolarizes the postsynaptic membrane or stabilizes it away from threshold, reducing the likelihood of firing an action potential.
The effect on the postsynaptic membrane depends on the sum of EPSPs and IPSPs from all presynaptic inputs, not on a single channel event.
The more negative the resting potential of the postsynaptic cell (i.e., the farther from threshold), the greater the depolarization needed to reach threshold, impacting how EPSPs translate to action potentials.
The analogy used in the lecture (e.g., touching a phone to a surface) illustrates how direct stimulation can affect the membrane potential, though actual signaling at chemical synapses involves neurotransmitters and receptor binding.
Neuromuscular and Neural Illustrations
Two primary cell types discussed: nerve cells (neurons) and muscle cells.
The connection between a nerve and a muscle cell occurs at the neuromuscular junction with a synapse-like structure across the synaptic cleft.
An action potential generated in a nerve cell leads to muscle contraction via signaling across this synapse, contributing to actions like blinking, contraction of muscles, and heart activity.
Heartbeat and muscle contractions are driven by action potentials and the propagation of electrical signals across cardiac and skeletal muscle tissues.
The overall picture emphasizes that action potentials underlie rapid responses and behavior, whereas EPSPs/IPSPs influence whether those action potentials occur in target cells.
Practical Implications and Takeaways
Resting membrane potential is kept by ion gradients and selective membrane conductances, with Na⁺/K⁺ ATPase contributing to maintaining gradients.
When a depolarizing stimulus reaches the threshold (~V_m = -50\ \text{mV}), a rapid, large inward Na⁺ current causes a spike in membrane potential toward the peak (~+40\ \text{mV}).
The peak is limited by the equilibrium potential of Na⁺ (around E_{Na} \approx +30\text{ to }+40\ \text{mV}); once near peak, K⁺ channels open, driving repolarization and often hyperpolarization before returning to RMP.
The process is not the result of a single ion channel opening but the coordinated opening of thousands of channels.
EPSPs promote depolarization toward threshold, while IPSPs counteract it; the net effect determines if an action potential is produced.
Understanding these concepts helps explain physiological phenomena such as blinking, contraction, and heart rhythms, illustrating the real-world relevance of membrane potential dynamics.