Neuron Resting Potential

The neuron resting potential is essential for understanding membrane potential changes like graded potentials and action potentials.

Components of the neuron:
- Soma (cell body) - denoted in red.
- Axon - denoted in green.
- Dendrite - denoted in blue (drawn larger for illustration).

The formation of neuron resting potential can be envisioned in sequential steps, though these processes happen simultaneously in reality.

Assumption: A neuron with no resting potential (no difference in ion concentration inside vs. outside).
Key ions: Organic anions, potassium (K extsuperscript{+}), sodium (Na extsuperscript{+}), chloride (Cl extsuperscript{-}), calcium (Ca extsuperscript{2+}).

As organic anions (mostly negatively charged proteins) are produced, the interior of the neuron becomes slightly more negative (e.g., about -5 mV).
- This small membrane potential does not enable neuron functionality yet.
- An electrical force attracts organic anions outwards while a diffusion force promotes their retention due to higher internal concentrations.
- However, organic anions cannot leave the neuron due to the membrane's high impermeability to them.

The neuron has leak channels, which are always open and allow for certain ions to pass through the membrane at varying rates.
- Different ions have varying ease of passage through these channels.

Introduction of the sodium-potassium pump (an active transporter):
- Transports 3 sodium ions outside the neuron and 2 potassium ions inside using energy from one ATP molecule.
- This action increases membrane potential, making it more negative (example value: around -10 mV).
- The significant effect is on ion concentrations within the neuron:
- Increased concentration of K extsuperscript{+} inside.
- Decreased concentration of Na extsuperscript{+} inside.
Reason for concentration differences: The extracellular fluid's vast volume means shifts in the neuron have a negligible impact on external concentrations.

Electrical force attempts to pull K extsuperscript{+} ions inside (attracted to negativity).
Diffusion force pushes K extsuperscript{+} ions outwards.
Typically, at neuron ion concentrations, diffusion force > electrical force:
- Leads to net K extsuperscript{+} outflow through leak channels.
- Resulting in increased negativity inside the neuron with each K ion that leaves until equilibrium potential is reached (approximately -70 mV).
- This state is termed the equilibrium potential (or reversal potential).
Very few K extsuperscript{+} need to leave (less than 0.01% of total K extsuperscript{+}) to reach this potential.

Both diffusion and electrical forces drive Na extsuperscript{+} into the neuron.
If Na extsuperscript{+} concentrations remain unchanged, their influx would eventually disrupt the negative internal environment, potentially positivity beyond -50 mV.
Under resting conditions, Na extsuperscript{+} permeability is significantly lower (around 4% permeable) compared to K extsuperscript{+}, which lessens its impact on resting potential (estimated around -60 mV).

Resulting membrane potential depends on the average of equilibrium potentials weighted by ion permeabilities.
Since resting membrane permeability leans heavily towards K extsuperscript{+}, resting potential is closer to K extsuperscript{+} equilibrium.

Although both Na extsuperscript{+} and K extsuperscript{+} generate small currents due to their movements across the membrane, the sodium-potassium pump continuously maintains these concentration gradients over time to ensure stability of the resting potential.

Chloride ions (Cl extsuperscript{-}) have a permeability of about 45% compared to K extsuperscript{+}.
Their concentration gradient is also influenced by the resting membrane potential:
- Ejection of Cl extsuperscript{-} by the membrane potential until balance is achieved, usually resulting in Cl extsuperscript{-} equilibrium near -60 mV.
- Active mechanisms like chloride-potassium symporter decrease intracellular Cl extsuperscript{-}, sending it out utilizing the potassium diffusion force.

Cl extsuperscript{-} equilibrium is generally close to -70 mV, potentially inducing slight inward Cl extsuperscript{-} flow, marginally affecting the overall resting potential.

Calcium ion concentrations are actively kept low inside the neuron by mechanisms such as the sodium-calcium exchanger, which trades Na extsuperscript{+} influx for Ca extsuperscript{2+} efflux.
The equilibrium potential for Ca extsuperscript{2+} is approximately +120 mV, highlighting strong inward forces on Ca extsuperscript{2+} under normal conditions.
Low resting membrane permeability to Ca extsuperscript{2+} means its impact on resting potential is typically minor.

While chloride and calcium links are minimal in the context of resting potential, they are crucial for other neuronal functions and will be further explored in subsequent discussions.