From cell to circuit

Neurons and synapses

Follow an electrical spike, cross a synapse and learn how transmitters and plasticity shape neural circuits.

Action potential

A brief all-or-none electrical event carries information along an axon.

Action-potential voltage trace

Chemical synapse

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Arrival

Action potential reaches the axon terminal.

Chemical synapse — step by step

Cells

Neuron anatomy

A neuron receives, integrates and transmits information through specialised parts.

Dendrites receive inputs.
The soma maintains the cell and integrates signals.
The axon carries output to terminals.

Glia

Glia support, insulate, nourish and defend neural circuits—and actively shape signaling.

Astrocytes regulate ions, transmitters and blood flow.
Oligodendrocytes make central myelin; Schwann cells myelinate peripheral nerves.
Microglia are resident immune cells.

Electrical signaling

Resting membrane potential

Ion gradients and selective membrane permeability keep a resting neuron near −70 mV.

K⁺ leak channels dominate resting permeability.
The Na⁺/K⁺ pump maintains gradients over time.

Refractory period

After a spike, channel states briefly prevent or resist another spike.

The absolute phase reflects Na⁺-channel inactivation.
The relative phase needs a stronger input while K⁺ conductance remains high.

Saltatory conduction

Myelin lets action potentials regenerate at nodes of Ranvier, speeding conduction.

Myelin reduces current loss across the axon membrane.
Demyelination slows or blocks transmission.

Synaptic chemistry

Electrical synapse

Gap junctions pass ionic current directly between cells with very little delay.

Often bidirectional.
Useful for synchronising groups of neurons.

Networks and integration

Postsynaptic potentials

Small EPSPs and IPSPs combine across space and time at the axon hillock.

EPSPs make firing more likely; IPSPs make it less likely.
Spatial summation combines synapses; temporal summation combines closely timed inputs.
Crossing threshold at the axon hillock triggers an action potential.

Plasticity

Neuroplasticity

Experience and activity can change synaptic strength, circuit organisation and structure.

LTP and LTD strengthen or weaken synaptic transmission.
Hebbian plasticity links cells that are repeatedly active together.
Structural plasticity can remodel spines, synapses and axons.

Neurotransmitters and clinical links

	Effect	Role	Where used	Neurotransmitters and clinical links
Glutamate	Excitatory	Main fast excitatory transmitter; central to learning and plasticity.	Widespread cortex and brain circuits.	Excess excitation can contribute to seizures and excitotoxic injury.
GABA	Inhibitory	Main fast inhibitory transmitter; stabilises circuit activity.	Interneurons throughout brain; cerebellar outputs.	Excitation–inhibition imbalance is relevant to epilepsy and anxiety treatments.
Dopamine	Modulatory	Shapes movement, reward learning, motivation and attention.	Nigrostriatal, mesolimbic and prefrontal pathways.	Nigrostriatal loss is central to Parkinson's; dopamine also signals reward prediction, not pleasure alone.
Serotonin	Modulatory	Modulates mood, sleep, appetite and behavioural flexibility.	Raphe projections reach much of the brain.	Many mood treatments target serotonin signaling, but low serotonin alone is not a diagnosis or complete explanation.
Acetylcholine	Modulatory	Supports attention, learning, memory and neuromuscular transmission.	Basal forebrain, brainstem and motor neurons.	Basal-forebrain cholinergic loss occurs in Alzheimer's; some treatments enhance cholinergic signaling.
Norepinephrine	Modulatory	Adjusts arousal, vigilance, stress responses and attention.	Locus coeruleus projections throughout cortex.	Targeted by some ADHD and depression medicines; effects depend on circuit and dose.
Glycine	Inhibitory	Fast inhibition in spinal cord and brainstem; also co-activates NMDA receptors.	Spinal cord, brainstem and NMDA synapses.	Disrupted glycine signaling can cause exaggerated startle and motor symptoms.
Endorphins	Modulatory	Endogenous opioid peptides that modulate pain, stress and reward.	Hypothalamic, pituitary and distributed pain circuits.	Opioid drugs recruit related receptors, creating analgesia as well as dependence and overdose risk.