Cellular and Synaptic Basis of Neural Signaling Flashcards

Vocabulary flashcards cover fundamental electrophysiology concepts, ion channel types, neurotransmitters, clinical channelopathies, and modern neuromodulation therapies, providing a comprehensive review of the cellular and synaptic basis of neural signaling.

Neuronal Excitability

The ability of neurons to generate and transmit electrical signals by regulated ion flow across the membrane.

Leak (Nongated) Ion Channel

Membrane channel that is open at rest, helping set and maintain the resting membrane potential.

Gated Ion Channel

Channel that opens or closes in response to voltage changes, chemical ligands, or intracellular messengers.

Voltage-Gated Sodium (Na⁺) Channel

Rapidly activating channel that initiates the action-potential upstroke and supports all-or-none signaling.

Saltatory Conduction

Rapid action-potential propagation in myelinated axons where impulses ‘jump’ between Nodes of Ranvier.

Voltage-Gated Calcium (Ca²⁺) Channel

Depolarization-activated channel at synaptic terminals whose Ca²⁺ influx triggers neurotransmitter release.

Ligand-Gated Ion Channel (Ionotropic Receptor)

Receptor that directly opens an ion pore when a neurotransmitter binds, producing fast synaptic currents.

G-Protein-Coupled Receptor (GPCR)

Seven-transmembrane receptor that modulates ion channels and signaling cascades via G-proteins.

Resting Membrane Potential (RMP)

Steady negative voltage across the neuronal membrane, primarily set by K⁺ permeability (~-70 mV).

Potassium (K⁺) Leak Channel

Selective channel whose continual K⁺ efflux dominates the resting potential.

Nernst (Equilibrium) Potential

Voltage at which an ion’s chemical and electrical driving forces are balanced (E_K ≈ −90 mV).

Sodium-Potassium ATPase

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

Hyperpolarization

Change that makes the membrane potential more negative, often via K⁺ efflux or Cl⁻ influx.

Depolarization

Membrane potential shift toward positive values, typically via Na⁺ or Ca²⁺ influx.

Membrane Capacitance (C_m)

Ability of the lipid bilayer to store charge between intra- and extracellular fluids.

Threshold Potential

Voltage (≈-45 to -30 mV) at which inward Na⁺ current surpasses leak currents, triggering an action potential.

Positive Feedback in AP Initiation

More Na⁺ entry causes further depolarization, which opens additional Na⁺ channels, accelerating the spike.

Repolarization

Phase in which Na⁺ channels inactivate and K⁺ channels open, driving the membrane back toward rest.

Afterhyperpolarization (Undershoot)

Transient period when membrane potential becomes more negative than rest due to prolonged K⁺ conductance.

Absolute Refractory Period

Interval after an action potential when no stimulus can evoke another spike because Na⁺ channels are inactivated.

Relative Refractory Period

Phase during which a stronger-than-normal depolarization is required to fire a new action potential; K⁺ channels still open.

Axon Hillock

Specialized initial segment where action potentials are first generated due to high Na⁺ channel density.

Passive (Electrotonic) Conduction

Signal spread that decays with distance, typical of dendritic postsynaptic potentials.

Myelin Sheath

Insulating glial membrane that raises resistance and lowers capacitance, speeding axonal conduction.

Node of Ranvier

Gap between myelin segments containing concentrated voltage-gated Na⁺ channels for AP regeneration.

Demyelinating Disease

Pathology (e.g., Multiple Sclerosis, Guillain-Barré) that disrupts myelin and slows or blocks conduction.

Voltage-Gated Ion Channel

Protein that opens in response to membrane voltage changes to permit selective ion flow.

Nav1.x Alpha Subunit

Pore-forming component of neuronal sodium channels responsible for fast Na⁺ conductance.

Tetrodotoxin (TTX)

Potent marine toxin that blocks the pore of most voltage-gated Na⁺ channels.

Carbamazepine

Antiepileptic drug that inhibits Na⁺ channels, stabilizing neuronal firing.

Voltage-Gated Potassium (K_v) Channel

Channel family that repolarizes the action potential and shapes firing patterns.

Delayed Rectifier K⁺ Channel

Kv subtype that opens during AP repolarization to return the membrane toward EK.

A-Type K⁺ Channel

Fast-inactivating K⁺ channel that controls interspike intervals and dendritic integration.

M-Channel (KCNQ2/3)

Slowly activating K⁺ channel; mutations cause neonatal epilepsy and influence neuronal excitability.

BK (Big-Conductance) Ca²⁺-Activated K⁺ Channel

Channel activated by both voltage and Ca²⁺ that contributes to afterhyperpolarization.

HCN Channel

Hyperpolarization-activated cyclic nucleotide-gated channel that carries pacemaker I_h current.

Voltage-Gated Calcium (Ca_v) Channel

Channel family mediating Ca²⁺ entry for neurotransmitter release and gene regulation.

T-Type Ca²⁺ Channel (Cav3.x)

Low-voltage-activated channel involved in rhythmic burst firing and thalamic oscillations.

L-Type Ca²⁺ Channel (Cav1.x)

High-voltage-activated channel with slow inactivation; target of dihydropyridine drugs.

N-Type Ca²⁺ Channel (Cav2.2)

Presynaptic channel critical for neurotransmitter release; blocked by ω-conotoxin.

P/Q-Type Ca²⁺ Channel (Cav2.1)

Channel abundant in cerebellum; CACNA1A mutations cause familial hemiplegic migraine.

R-Type Ca²⁺ Channel (Cav2.3)

High-voltage channel contributing to excitatory synaptic transmission; less well understood.

Voltage-Gated Chloride (ClC) Channel

Channel family controlling muscle and neuronal excitability; ClC-1 defects cause myotonia.

CFTR

ATP-gated Cl⁻ channel whose mutations lead to cystic fibrosis.

GABA_A Receptor

Ligand-gated Cl⁻ channel mediating fast inhibitory neurotransmission in the CNS.

Glycine Receptor

Spinal cord inhibitory Cl⁻ channel that reduces neuronal firing.

Cyclic Nucleotide-Gated (CNG) Channel

Channel gated by cAMP/cGMP; crucial for visual and olfactory transduction.

Transient Receptor Potential (TRP) Channel

Large channel family mediating sensory detection of temperature, pain, and touch.

Voltage-Dependent Anion Channel (VDAC)

Mitochondrial pore controlling metabolite exchange and apoptosis pathways.

Glutamate

Primary excitatory neurotransmitter that activates AMPA, NMDA, and kainate receptors.

Acetylcholine (ACh)

Excitatory transmitter at neuromuscular junctions and many CNS synapses.

GABA (γ-Aminobutyric Acid)

Major inhibitory neurotransmitter that opens Cl⁻ channels to hyperpolarize neurons.

Glycine

Spinal cord and brainstem inhibitory transmitter activating Cl⁻ channels.

Biogenic Amine

Modulatory neurotransmitter class including dopamine, norepinephrine, serotonin, and histamine.

Ionotropic vs. Metabotropic

Direct ligand-gated ion flow versus indirect GPCR-mediated channel modulation.

Excitatory Postsynaptic Potential (EPSP)

Depolarizing synaptic potential that increases the probability of firing an action potential.

Inhibitory Postsynaptic Potential (IPSP)

Hyperpolarizing synaptic potential that decreases neuronal excitability.

Cys-Loop Receptor

Pentameric ionotropic receptor family (nAChR, GABA_A, GlyR, 5-HT3) with a characteristic disulfide loop.

AMPA Receptor

Fast glutamate-gated cation channel responsible for most rapid excitatory synaptic transmission.

NMDA Receptor

Voltage- and ligand-gated glutamate receptor permeable to Ca²⁺; key for synaptic plasticity.

Kainate Receptor

Glutamate receptor mediating slower excitatory currents and modulatory roles.

P2X Receptor

ATP-gated cation channel involved in fast purinergic signaling and pain pathways.

Metabotropic Glutamate Receptor (mGluR)

GPCR that modulates synaptic plasticity and neuronal excitability through second messengers.

Oscillatory Neuronal Firing

Rhythmic activity patterns that underlie behaviors such as sleep, attention, and mood.

Thalamocortical Oscillation

LVA Ca²⁺-dependent rhythm generating EEG sleep spindles; disruptions lead to absence epilepsy.

Excitation/Inhibition (E/I) Balance

Dynamic equilibrium between glutamatergic and GABAergic activity critical for normal cognition.

Channelopathy

Disease caused by dysfunctional ion channels due to genetic mutation or autoimmunity.

Benign Familial Neonatal Convulsions (BFNC)

Epileptic disorder from KCNQ2/3 mutations affecting M-channels.

GEFS+

Genetic epilepsy with febrile seizures plus, often linked to Na⁺ channel mutations.

CACNA1A Mutation

Genetic alteration in P/Q-type Ca²⁺ channels causing migraine or ataxia syndromes.

SCN9A Mutation

Na_v1.7 channel defect producing extreme pain disorder or congenital insensitivity to pain.

Anti-NMDA Receptor Encephalitis

Autoimmune condition with antibodies against NMDA receptors causing psychosis and seizures.

Hebbian Plasticity

Activity-dependent strengthening or weakening of synapses (LTP/LTD) underlying learning.

Homeostatic Plasticity

Compensatory adjustment of synaptic strength to stabilize overall neuronal activity.

Electroconvulsive Therapy (ECT)

Clinical induction of seizures via electrical stimulation to treat severe depression.

Deep Brain Stimulation (DBS)

Implanted electrode therapy delivering high-frequency pulses to modulate neural circuits.

Repetitive Transcranial Magnetic Stimulation (rTMS)

Noninvasive brain stimulation using repeated magnetic pulses to alter cortical excitability.

Vagus Nerve Stimulation (VNS)

Implanted device that periodically activates vagal afferents for epilepsy and depression treatment.

Optogenetics

Technique that uses light-activated ion channels to precisely control genetically defined neurons.

Chemogenetics

Use of engineered, drug-responsive ion channels or GPCRs to modulate specific neural circuits.