Neural Communication: Neurons, Action Potentials & Synaptic Transmission

All 10 Terms & Definitions

Neuron structure

A typical neuron has four functional regions. Soma (cell body): contains nucleus and metabolic machinery; synthesises proteins. Dendrites: branching processes that receive synaptic input from other neurons; expanded by dendritic spines. Axon: single elongated process that conducts action potentials away from the soma; may be myelinated; branches terminally. Axon hillock: junction of soma and axon where action potentials are initiated (lowest threshold). Synaptic boutons (terminals): release neurotransmitters onto target cells.

Neuron types

Three functional types: (1) Sensory (afferent) neurons — detect stimuli and transmit information toward the CNS; cell bodies in dorsal root ganglia or cranial nerve ganglia. (2) Motor (efferent) neurons — carry commands from CNS to effectors (skeletal muscle in somatic system; smooth muscle, cardiac muscle, glands in autonomic system). (3) Interneurons — ~99% of all CNS neurons; connect sensory and motor pathways, integrate information, and mediate all complex processing and cognition.

Glial cells

Non-neuronal support cells of the nervous system. Astrocytes (CNS): maintain blood-brain barrier, regulate extracellular K+ and neurotransmitter concentrations, provide metabolic support, form tripartite synapses. Oligodendrocytes (CNS): myelinate multiple axons; loss causes multiple sclerosis. Schwann cells (PNS): myelinate individual axons; support peripheral nerve regeneration. Microglia: CNS immune cells — phagocytose debris, mediate neuroinflammation. Ependymal cells: line ventricles; produce and circulate CSF.

Resting membrane potential

The electrical potential across the neuronal membrane at rest: approximately −70 mV (inside negative). Arises from selective K+ permeability (K+ leak channels allow K+ to flow out down its concentration gradient, leaving negative charge inside) and the Na+/K+ ATPase (pumps 3 Na+ out and 2 K+ in per ATP, maintaining high [K+] inside and high [Na+] outside). The actual resting potential is more positive than the K+ equilibrium potential (EK ≈ −90 mV) because of slight Na+ permeability.

Action potential

An all-or-none electrical signal propagated along the axon. When depolarisation at the axon hillock reaches threshold (~−55 mV): (1) voltage-gated Na+ channels open → rapid Na+ influx → depolarisation to ~+40 mV; (2) Na+ channels inactivate (absolute refractory period) AND voltage-gated K+ channels open → K+ efflux → repolarisation; (3) K+ channels close slowly → brief afterhyperpolarisation (relative refractory period). Restored by Na+/K+ ATPase. Duration: ~1–2 ms.

Saltatory conduction

Rapid action potential propagation in myelinated axons. Myelin reduces membrane capacitance and increases internode resistance, so depolarisation current flows efficiently along the axon interior from one node of Ranvier to the next, where the action potential is regenerated. The AP "jumps" between nodes (saltare = to jump), dramatically increasing velocity: myelinated Aα fibres 70–120 m/s; unmyelinated C fibres 0.5–2 m/s. Loss of myelin (multiple sclerosis, Guillain-Barré) disrupts conduction.

Synaptic transmission

Conversion of electrical signals into chemical messages at the synapse. Sequence: AP arrives at presynaptic terminal → voltage-gated Ca2+ channels open → Ca2+ influx → synaptotagmin/SNARE complex drives synaptic vesicle fusion → neurotransmitter exocytosed into the cleft (~20 nm wide) → NT diffuses across → binds to postsynaptic receptors. Ionotropic receptors (ligand-gated ion channels): fast response (ms). Metabotropic receptors (G-protein-coupled): slow, modulatory response (100s of ms to seconds).

EPSP and IPSP

Postsynaptic potentials (graded, not all-or-none). EPSP (excitatory postsynaptic potential): a transient depolarisation that moves the membrane toward threshold; typically caused by glutamate on AMPA receptors (Na+ influx). IPSP (inhibitory postsynaptic potential): a transient hyperpolarisation or conductance increase that moves the membrane away from threshold; typically caused by GABA on GABA-A receptors (Cl− influx). Summation: temporal (rapid successive EPSPs add) and spatial (EPSPs from multiple inputs add) — integrated at the axon hillock.

Neurotransmitters

Chemical messengers released at synapses. Major types: Glutamate — primary excitatory NT in CNS; acts on AMPA (fast Na+/Ca2+), NMDA (Ca2+; plasticity), and kainate receptors. GABA — primary inhibitory NT in CNS; acts on GABA-A (Cl− influx) and GABA-B (metabotropic). Dopamine — reward, motor control, executive function. Serotonin — mood, sleep, appetite. Acetylcholine — neuromuscular junction, autonomic ganglia, memory. Noradrenaline — arousal, attention, stress.

NT termination (reuptake & degradation)

Mechanisms that end neurotransmitter signalling: (1) Reuptake: transporter proteins (SERT for serotonin, DAT for dopamine, NET for noradrenaline, GAT for GABA, EAATs for glutamate) remove NT from the cleft into presynaptic terminal or glia for repackaging. (2) Enzymatic degradation: acetylcholinesterase cleaves ACh in the cleft; MAO and COMT degrade monoamines intracellularly after reuptake. (3) Diffusion: NT molecules disperse from the cleft. Drug targets: SSRIs block SERT; cocaine blocks DAT; acetylcholinesterase inhibitors used in Alzheimer's disease.