## Ion Selectivity at the Neuromuscular Junction ### The Acetylcholine Receptor Channel **Key Point:** The nicotinic acetylcholine receptor (nAChR) at the neuromuscular junction is a non-selective cation channel that permits the passage of both Na⁺ and K⁺, but the **net inward current is driven by Na⁺ influx**, which depolarizes the membrane. ### Ion Gradient Driving Forces | Ion | Extracellular | Intracellular | Equilibrium Potential | Direction | |-----|---------------|---------------|----------------------|----------| | Na⁺ | ~145 mM | ~12 mM | +60 mV | **Inward** | | K⁺ | ~5 mM | ~150 mM | −90 mV | Outward | | Cl⁻ | ~110 mM | ~4 mM | −70 mV | Inward | | Ca²⁺ | ~2 mM | ~0.1 μM | +120 mV | Inward | **High-Yield:** At the resting membrane potential (~−70 mV), the driving force for Na⁺ is much larger than for K⁺. Although both ions flow through the open nAChR channel, the **Na⁺ influx dominates**, producing a net inward (depolarizing) current. ### Mechanism of Depolarization **Mnemonic:** **SNAP** — **S**odium influx **N**eutralizes **A**nion **P**otential 1. ACh binds to nAChR → channel opens 2. Na⁺ rushes in (down its electrochemical gradient) 3. K⁺ leaks out (but at a slower rate) 4. Net inward current → membrane depolarization → end-plate potential (EPP) 5. If EPP exceeds threshold, an action potential is triggered ### Why Not Other Ions? **Clinical Pearl:** Although Ca²⁺ has the largest equilibrium potential (+120 mV), it is **not the primary ion** responsible for depolarization at the NMJ because: - The nAChR has low Ca²⁺ permeability relative to Na⁺ - The driving force for Na⁺ is sufficient to depolarize the membrane - Excessive Ca²⁺ influx would trigger unwanted intracellular signaling K⁺ efflux opposes depolarization, and Cl⁻ is excluded by the negative charge inside the cell. [cite:Kandel et al. Principles of Neural Science 6e Ch 11]
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