Which ion is responsible for the depolarization phase of the postsynaptic potential at an excitatory synapse?

Explanation

## Ion Flux in Excitatory Synaptic Transmission **Key Point:** Sodium ions (Na⁺) influx through ligand-gated ion channels is the primary driver of depolarization at excitatory synapses, generating the excitatory postsynaptic potential (EPSC). ### Mechanism of EPSC Generation 1. **Neurotransmitter binding** (e.g., acetylcholine at nicotinic receptors) opens Na⁺/K⁺ channels 2. **Sodium influx** dominates because: - Na⁺ equilibrium potential (~+60 mV) is far from resting potential (~−70 mV) - Na⁺ concentration gradient is steep (outside >> inside) - Channel conductance to Na⁺ is high when open 3. **Membrane depolarization** occurs (from −70 mV toward +20 to +30 mV) 4. **EPSP magnitude** typically 0.5–1 mV per quantum of transmitter ### Ionic Driving Force $$V_m - E_{Na} = \text{Driving force for Na}^+$$ Where $V_m$ (membrane potential) is more negative than $E_{Na}$ (sodium equilibrium potential), Na⁺ flows inward. **High-Yield:** At the neuromuscular junction, the reversal potential of the nicotinic EPSC is approximately 0 mV (where Na⁺ and K⁺ currents balance), confirming dual-cation permeability but Na⁺ dominance in depolarization. ### Contrast with Inhibitory Synapses - **IPSC:** Cl⁻ influx or K⁺ efflux → hyperpolarization (away from threshold) - **Inhibitory neurotransmitters:** GABA, glycine → open Cl⁻ or K⁺ channels **Mnemonic:** **ERICA** = Excitatory = Inward (Na⁺) = Cation = Depolarization