Resting membrane potential
Also known as: RMP, resting potential, Nernst potential, equilibrium potential
The steady voltage across the membrane of an unstimulated neuron, inside negative relative to outside, typically ≈ −70 mV. It arises mainly from K⁺ leaking out down its concentration gradient through K⁺ leak channels, and the Na⁺/K⁺-ATPase maintains the gradients.
Overview
Two conditions create the potential: unequal ion distributions across the membrane and selective permeability to those ions. The Na⁺/K⁺-ATPase pumps 3 Na⁺ out and 2 K⁺ in per ATP, so K⁺ is concentrated inside (≈140 mM) and Na⁺ outside (≈145 mM). At rest the membrane is far more permeable to K⁺ (≈25–100×) than to Na⁺, because of K⁺ leak channels: two-pore-domain (K2P) and inward-rectifier channels. As K⁺ diffuses out it leaves behind impermeant intracellular anions, mostly proteins and organic phosphates. This builds an inside-negative potential that opposes further efflux.
For a single ion, the Nernst equation gives the equilibrium potential at which the electrical and chemical forces balance. At 37 °C, E = 61.5/z × log₁₀([ion]out/[ion]in) mV. E_K ≈ −90 to −95 mV, E_Na ≈ +60 mV, E_Cl ≈ −70 mV and E_Ca ≈ +120 mV. The resting potential lies close to E_K but is somewhat less negative, because of a small Na⁺ leak. The Goldman–Hodgkin–Katz equation expresses this, weighting each ion by its permeability. The pump's own electrogenic contribution is small (≈ −4 mV directly); its main role is to maintain the gradients over time.
The RMP determines excitability. Moving it toward threshold (≈ −55 mV) makes the cell easier to fire. Different cells have different values: neurons ≈ −70 mV; skeletal and ventricular muscle ≈ −90 mV; smooth muscle ≈ −50 to −60 mV; and sinoatrial node cells have no stable RMP (≈ −60 mV maximum diastolic potential).
Parts & subdivisions
- Na⁺ (out ≈145 / in ≈12–15 mM)E_Na ≈ +60 mV. Low resting permeability. The large inward driving force powers the upstroke of the action potential.
- K⁺ (out ≈4–5 / in ≈140 mM)E_K ≈ −90 to −95 mV. High resting permeability through leak channels, so K⁺ is the main determinant of the RMP.
- Cl⁻ (out ≈110 / in ≈7–10 mM)E_Cl ≈ −70 mV, close to the RMP in mature neurons (set by the KCC2 transporter). Opening Cl⁻ channels (GABA-A, glycine) therefore clamps the membrane and inhibits. In immature neurons (NKCC1, high internal Cl⁻), GABA is depolarising.
- Ca²⁺ (out ≈1.2 mM free / in ≈0.0001 mM)E_Ca ≈ +120 mV. Intracellular free Ca²⁺ is kept extremely low by pumps and exchangers, so Ca²⁺ entry serves as a signal (transmitter release, muscle contraction).
- Na⁺/K⁺-ATPaseElectrogenic pump moving 3 Na⁺ out and 2 K⁺ in per ATP. It consumes a large share of the brain's energy, maintains the gradients and adds a few mV of negativity. Inhibited by ouabain and digoxin.
Function
- Stores electrochemical energy used for signalling.
- Sets neuronal excitability and threshold distance.
- Provides the gradients that drive secondary active transport (glutamate uptake, Na⁺–Ca²⁺ exchange).
- Physiology
Raising extracellular K⁺ makes E_K, and thus the RMP, less negative. A sustained depolarisation inactivates voltage-gated Na⁺ channels, so after a brief rise in excitability the cell becomes less excitable. Lowering extracellular K⁺ hyperpolarises the cell and makes it harder to excite.
Clinical significance
Hyperkalaemia and hypokalaemia
Hyperkalaemia depolarises the RMP. This first increases excitability, then inactivates Na⁺ channels, causing muscle weakness and paralysis and dangerous cardiac changes (peaked T waves, widened QRS, sine wave, asystole). Calcium gluconate stabilises the myocardium. Hypokalaemia hyperpolarises nerve and muscle, causing weakness, ileus, U waves and arrhythmias.
Compiled from standard anatomy and physiology references — see the Nervous System sources. For education only; not medical advice.