Membrane Electrophysiology & Action Potentials – Vocabulary Review

A comprehensive set of vocabulary flashcards covering ion channels, membrane potentials, action potentials, refractory periods, conduction mechanisms, synaptic physiology, and clinical electrolyte imbalances.

Membrane Potential (Vm)

The voltage difference across a cell membrane resulting from unequal distribution of ions.

Equilibrium Potential (Eion)

The membrane voltage at which the electrical and chemical gradients for a specific ion are balanced; calculated with the Nernst equation.

Resting Membrane Potential (RMP)

The steady-state membrane potential (≈ –70 mV in neurons) established mainly by K⁺ leak and the Na⁺/K⁺-ATPase.

Na⁺/K⁺-ATPase (Sodium-Potassium Pump)

Active transporter that moves 3 Na⁺ out and 2 K⁺ into the cell per ATP, helping maintain ion gradients and RMP.

Leak Channel

Non-gated ion channel that is always open; K⁺ leak channels dominate and set RMP.

Voltage-Gated Sodium Channel (VG Na⁺)

Channel that rapidly opens at threshold to allow Na⁺ influx, causing the AP upstroke; inactivates quickly.

Voltage-Gated Potassium Channel (VG K⁺)

Channel that opens more slowly during an AP, allowing K⁺ efflux to repolarize and hyperpolarize the membrane.

Threshold Potential

Membrane voltage (≈ –55 mV) at which enough VG Na⁺ channels open to trigger an action potential.

Depolarization

Movement of Vm toward more positive values, usually via Na⁺ or Ca²⁺ influx.

Repolarization

Return of Vm toward RMP after depolarization, typically via K⁺ efflux.

Hyperpolarization

Vm becomes more negative than RMP, often due to prolonged K⁺ efflux or Cl⁻ influx.

Action Potential (AP)

A rapid, all-or-none reversal of membrane polarity that propagates along excitable membranes.

Absolute Refractory Period

Time during which no second AP can occur because VG Na⁺ channels are inactivated.

Relative Refractory Period

Period when a stronger stimulus is needed for an AP because some VG Na⁺ have reset but VG K⁺ remain open.

Saltatory Conduction

AP propagation that ‘jumps’ between nodes of Ranvier in myelinated axons, increasing speed and efficiency.

Contiguous Conduction

Slower AP propagation along every segment of an unmyelinated axon.

Myelination

Insulation of axons by glial cell membranes (Schwann/oligodendrocytes) that increases conduction velocity.

Graded Potential

Small, local change in Vm that varies with stimulus strength and can summate but decays with distance.

Spatial Summation

Addition of simultaneous graded potentials from different locations on the neuron.

Temporal Summation

Addition of graded potentials that arrive in rapid succession at one location.

EPSP (Excitatory Postsynaptic Potential)

Graded depolarization that moves Vm closer to threshold, often via Na⁺ or Ca²⁺ influx.

IPSP (Inhibitory Postsynaptic Potential)

Graded hyperpolarization that moves Vm farther from threshold, typically via Cl⁻ influx or K⁺ efflux.

Glutamate

Major excitatory neurotransmitter; opens ligand-gated cation channels (AMPA/NMDA) allowing Na⁺ and Ca²⁺ influx → EPSP.

GABA

Primary inhibitory neurotransmitter; opens GABA_A Cl⁻ channels causing Cl⁻ influx → IPSP.

Hyperkalemia

Elevated extracellular K⁺ that depolarizes RMP, risking inexcitability due to impaired repolarization.

Hypokalemia

Low extracellular K⁺ that hyperpolarizes RMP, making threshold harder to reach.

Hypernatremia

High extracellular Na⁺; can slightly increase AP amplitude but mainly alters osmolarity.

Hyponatremia

Low extracellular Na⁺; can slightly reduce AP amplitude and cause cellular swelling.

Hypercalcemia

Elevated extracellular Ca²⁺ that stabilizes VG Na⁺ channels, reducing excitability and muscle spasm likelihood.

Hypocalcemia

Low extracellular Ca²⁺ that lowers VG Na⁺ activation threshold, increasing spontaneous nerve firing and tetany.

Hyperchloremia

High extracellular Cl⁻; can enhance Cl⁻ influx during IPSPs, promoting hyperpolarization.

Insulin-Mediated K⁺ Uptake

Insulin stimulates Na⁺/K⁺-ATPase, driving K⁺ into cells and lowering plasma K⁺—clinically used to treat hyperkalemia.

KCl Lethal Injection

Intravenous KCl raises extracellular K⁺ sharply, depolarizing cardiac cells and stopping repolarization → cardiac arrest.

Node of Ranvier

Unmyelinated axonal segment with high VG channel density where APs are regenerated in saltatory conduction.

All-or-None Principle

An AP occurs fully once threshold is crossed; its amplitude does not scale with stimulus strength.

Non-Decremental Conduction

AP amplitude remains constant as it propagates along the axon.

Synaptic Integration

Process by which a neuron sums all EPSPs and IPSPs to decide whether to fire an AP.

Voltage-Gated Channel Inactivation

Time-dependent closure of VG Na⁺ channels despite continued depolarization, producing the absolute refractory period.

Presynaptic Inhibition

Reduction in neurotransmitter release, often via GABAergic terminals acting on the presynaptic neuron.

Excitable Cell

Cell capable of generating APs (e.g., neurons, skeletal muscle fibers, cardiac myocytes).