Cognitive Connie
Neural Communication: Neurons, Action Potentials & Synaptic Transmission
Every thought, feeling, and behaviour depends on electrical and chemical signalling between neurons. At the cellular level, this involves maintaining a resting membrane potential, generating and propagating action potentials, and converting electrical signals into chemical messages at synapses — where neurotransmitters released from one neuron bind to receptors on another.
Key figures
Santiago Ramón y Cajal
1852–1934Spanish neuroscientist who, using Golgi's staining method, established the neuron doctrine: neurons are discrete cells communicating across gaps (synapses) rather than forming a continuous reticulum. Shared the Nobel Prize in Physiology or Medicine in 1906. His meticulous drawings of neural circuits remain landmark illustrations in neuroscience.
Bernard Katz
1911–2003German-British physiologist who established the quantal nature of neurotransmitter release: NT is released in discrete packets (quanta) corresponding to single synaptic vesicles. He also characterised the role of Ca2+ in triggering vesicle fusion at the neuromuscular junction. Shared the Nobel Prize in Physiology or Medicine in 1970.
Alan Hodgkin & Andrew Huxley
1914–1998 / 1917–2012British physiologists who used the squid giant axon to describe the ionic mechanisms of the action potential (1952), earning the Nobel Prize in Physiology or Medicine in 1963. Their Hodgkin-Huxley model — showing how voltage-gated Na+ and K+ channels generate and propagate the action potential — remains the foundation of computational neuroscience.
Key concepts
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.
Test your knowledge
Sources
Last reviewed July 2025- 1.
Hodgkin, A. L., & Huxley, A. F. (1952). A quantitative description of membrane current and its application to conduction and excitation in nerve. Journal of Physiology, 117(4), 500–544. https://doi.org/10.1113/jphysiol.1952.sp004764
+About this source
Nobel Prize-winning paper providing the mathematical model of the action potential based on voltage-gated ion channels in the squid giant axon.
- 2.
Katz, B. (1966). Nerve, Muscle, and Synapse. McGraw-Hill.
+About this source
Katz's concise account of synaptic transmission, the quantal nature of neurotransmitter release, and the role of calcium in vesicle fusion.
- 3.
Kandel, E. R., Schwartz, J. H., Jessell, T. M., Siegelbaum, S. A., & Hudspeth, A. J. (2021). Principles of Neural Science (6th ed.). McGraw-Hill.
+About this source
Definitive textbook covering neuron structure, neuron types, glial cells, resting potential, action potentials, and synaptic transmission mechanisms.