Cellular and Synaptic Basis of Neural Signaling – Key Vocabulary

Ion Channel

Membrane-spanning protein pore that allows specific ions to flow across the lipid bilayer.

Nongated (Leak) Channel

Ion channel that is open at rest and helps set the resting membrane potential.

Voltage-Gated Ion Channel

Channel whose opening/closing is controlled by changes in trans-membrane voltage.

Ligand-Gated Ion Channel

Channel that opens directly when a neurotransmitter binds to it.

G-Protein–Coupled Receptor (GPCR)

Seven-transmembrane receptor that signals via heterotrimeric G-proteins to modulate ion channels or second messengers.

Resting Membrane Potential

Stable negative membrane voltage (≈-55 to ‑70 mV in neurons) established by leak channels and ion gradients.

Equilibrium (Nernst) Potential

Membrane voltage at which the electrical and chemical gradients for a single ion are balanced; no net ion flux.

Goldmann–Hodgkin–Katz Equation

Formula that predicts the actual membrane potential based on multiple ions and their permeabilities.

Voltage-Gated Sodium Channel

Fast-activating, fast-inactivating channel (Nav) responsible for the upstroke of action potentials.

Action Potential

All-or-none, rapid depolarization–repolarization electrical signal that propagates along axons.

Threshold Potential

Membrane voltage at which inward Na+ current first exceeds leak current, triggering an action potential.

Overshoot

Portion of the action potential where membrane voltage becomes positive to 0 mV.

Afterhyperpolarization (AHP)

Transient membrane hyperpolarization following an action potential, often mediated by K+ channels.

Absolute Refractory Period

Interval after a spike when no new action potential can be generated due to Na+ channel inactivation.

Relative Refractory Period

Period following the absolute refractory period when a stronger-than-normal stimulus is needed to fire.

Axon Hillock

Initial segment of the axon where action potentials are typically generated.

Node of Ranvier

Unmyelinated axonal gap rich in voltage-gated Na+ channels; site of action-potential regeneration.

Saltatory Conduction

Rapid action-potential propagation in myelinated axons, jumping from node to node.

Voltage-Gated Calcium Channel

Depolarization-activated channel (Cav) whose Ca2+ influx triggers neurotransmitter release and other processes.

Patch Clamp

Electrophysiological technique that records currents through individual ion channels or whole cells.

Voltage Clamp

Method that holds membrane potential constant to isolate ionic currents for study.

Na+-K+ ATPase (Sodium Pump)

Electrogenic pump that moves 3 Na+ out and 2 K+ in, maintaining ion gradients and resting potential.

Delayed Rectifier K+ Channel

Voltage-gated K+ channel that activates after Na+ channels and helps repolarize the action potential.

BK Channel

Large-conductance Ca2+- and voltage-activated K+ channel mediating fast AHP.

SK Channel

Small-conductance Ca2+-activated K+ channel contributing to medium/slow AHP and spike frequency adaptation.

A-Type K+ Channel

Rapidly activating and inactivating K+ channel that controls interspike interval and excitability.

M-Channel (KCNQ)

Slowly activating K+ channel suppressed by muscarinic receptors; limits repetitive firing.

Inward Rectifier (Kir)

K+ channel that passes inward K+ current more easily than outward; stabilizes resting potential.

GIRK

G-protein–regulated inwardly rectifying K+ channel opened by transmitters like GABA and adenosine.

KATP Channel

ATP-sensitive Kir channel linking cellular metabolism to membrane excitability; target of sulfonylureas.

HCN (H-) Channel

Hyperpolarization-activated, cyclic-nucleotide–gated cation channel that mediates pacemaker Ih current.

K2P (Tandem-Pore) Channel

Four-TM, two-P-domain K+ channel providing background leak conductance (e.g., TASK, TRAAK, TWIK).

ASIC

Acid-sensing ion channel; voltage-insensitive cation channel activated by extracellular acidification.

Tetrodotoxin (TTX)

Puffer-fish toxin that blocks most voltage-gated Na+ channels extracellularly.

Saxitoxin (STX)

Algal toxin that blocks TTX-sensitive Na+ channels at an extracellular site.

Use-Dependent Block

Drug action that preferentially blocks channels in active or inactivated states (e.g., local anesthetics).

Retigabine

Anticonvulsant that opens KCNQ (M-) channels, reducing neuronal excitability.

Ethosuximide

Antiepileptic drug that inhibits T-type (LVA) Ca2+ channels, effective in absence seizures.

Lamotrigine

Anticonvulsant that inhibits Na+ channels and enhances HCN currents; also mood stabilizer.

Conotoxin GVIA

Snail toxin that irreversibly blocks N-type Ca2+ channels.

Prialt (Conotoxin MVIIA)

Synthetic peptide that reversibly blocks N-type Ca2+ channels for chronic pain relief.

Agatoxin IVA

Spider toxin that blocks P/Q-type Ca2+ channels.

LVA (T-Type) Ca2+ Channel

Low-voltage–activated, transient Ca2+ channel (Cav3) important for burst firing and oscillations.

HVA (High-Voltage–Activated) Ca2+ Channel

Ca2+ channel class (Cav1 & Cav2) requiring stronger depolarization; includes L-, N-, P/Q-, R-types.

L-Type Ca2+ Channel

Long-lasting HVA channel (Cav1) sensitive to dihydropyridines; couples activity to gene expression.

N-Type Ca2+ Channel

HVA channel (Cav2.2) that mediates transmitter release, blocked by conotoxins.

P/Q-Type Ca2+ Channel

HVA channel (Cav2.1) prominent in CNS synaptic release; mutations cause familial hemiplegic migraine.

R-Type Ca2+ Channel

Cav2.3 channel resistant to many blockers; contributes to CNS transmission.

Synprint Region

Intracellular loop on Cav2 channels that binds presynaptic proteins to modulate Ca2+ influx.

TRP Channel

Transient receptor potential family of Ca2+-permeable cation channels responsive to diverse stimuli.

Cystic Fibrosis Transmembrane Conductance Regulator (CFTR)

ABC family Cl− channel whose mutations cause cystic fibrosis; activated by PKA and ATP.

ClC Channel

Voltage-gated Cl− channel family; ClC-1 defects cause myotonia congenita.

Ca2+-Activated Cl− Channel

Channel that opens with intracellular Ca2+ rises, influencing firing frequency and volume regulation.

Voltage-Dependent Anion Channel (VDAC)

Mitochondrial porin that forms part of the permeability transition pore regulating apoptosis.

Neurotransmitter

Chemical messenger released from presynaptic terminals that binds receptors on target cells.

Excitatory Postsynaptic Potential (EPSP)

Depolarizing synaptic potential typically mediated by glutamate or acetylcholine receptors.

Inhibitory Postsynaptic Potential (IPSP)

Hyperpolarizing or shunting synaptic potential usually mediated by GABA or glycine receptors.

Hebbian Plasticity

Use-dependent synaptic modification requiring coincident pre- and postsynaptic activity (LTP/LTD).

Homeostatic Plasticity

Adaptive adjustment of synaptic strength or excitability to stabilize overall network activity.

Metaplasticity

Activity-dependent change in the ease of inducing subsequent Hebbian plasticity.

E/I Balance

Ratio of excitation to inhibition within a circuit; critical for normal network function.

Pacemaker (Intrinsic Oscillator)

Neuron whose membrane conductances allow rhythmic, spontaneous firing.

Burst Firing

Episodes of high-frequency spikes followed by quiescence, often increasing Ca2+ entry.

Channelopathy

Disease caused by mutations or dysfunction of ion channels.

SCN9A (Nav1.7)

Sodium channel gene whose mutations cause pain insensitivity or paroxysmal extreme pain disorder.

KCNQ2/3

Genes encoding M-channel subunits; mutations cause benign familial neonatal convulsions.

CACNA1A

Gene for Cav2.1 P/Q-type α1 subunit; mutations linked to familial hemiplegic migraine, episodic ataxia 2, SCA6.

Anti-NMDA Receptor Encephalitis

Autoimmune disorder with antibodies against GluN1 causing NMDAR hypofunction and psychiatric symptoms.

Electroconvulsive Therapy (ECT)

Clinical induction of generalized seizures via controlled electrical pulses to treat severe depression.

Repetitive Transcranial Magnetic Stimulation (rTMS)

Non-invasive brain stimulation using focused magnetic pulses to modulate cortical excitability.

Deep Brain Stimulation (DBS)

Implanted electrodes deliver continuous high-frequency pulses to modulate subcortical circuits.

Vagus Nerve Stimulation (VNS)

Chronic intermittent electrical stimulation of the vagus nerve used in refractory epilepsy and depression.

tDCS

Transcranial direct current stimulation; low-level current applied through scalp electrodes to alter cortical excitability.

Optogenetics

Technique using light-activated ion channels to control genetically targeted neurons.

Chemogenetics (DREADDs)

Use of engineered receptors activated by synthetic ligands to modulate specific neuron populations.

Use-Dependent Drug

Agent whose channel block increases with repetitive channel activation (e.g., phenytoin).

Tetrodotoxin-Insensitive Na+ Channel

Nav subtype (e.g., Nav1.5) that is resistant to TTX and contributes to certain pain pathways.

Delayed Rectification

Property of K+ channels that preferentially conduct outward current upon depolarization.

Synaptic Scaling

Global adjustment of synaptic strengths to stabilize firing rates during prolonged activity changes.

Gamma (