Neurons Course

Lesson 1 • The Neuron as a Cell

Neurons are specialised cells with unique structural features enabling electrical signalling. This section grounds all subsequent study in cellular anatomy.

Lesson 2 • Structural Components of Neurons

Soma, dendrites, and axons each serve distinct functional roles. Understanding these parts is essential for grasping signal transmission.

Lesson 3 • Glial Cells and Support Functions

Glial cells maintain the environment neurons require to function. Their roles in insulation, nutrition, and repair are foundational concepts.

Lesson 4 • Neuron Development and Lifespan

Neurons form through neurogenesis and mature via pruning and myelination. This section connects cellular biology to brain development over time.

Lesson 1 • The Resting Membrane Potential

A neuron at rest maintains a negative internal charge through ion distribution. This voltage difference is the baseline for all electrical signalling.

Lesson 2 • Ion Channels and Gating

Ion channels open and close in response to voltage, ligands, or mechanical stimuli. Channel behaviour directly controls membrane excitability.

Lesson 3 • The Action Potential

Action potentials are all-or-none electrical impulses propagated along the axon. Mastering their phases is central to understanding neural communication.

Lesson 4 • Graded Potentials

Graded potentials are local, variable-amplitude changes in membrane voltage. They integrate incoming signals before triggering an action potential.

Lesson 1 • Receptor Binding and Postsynaptic Response

Neurotransmitters bind ionotropic or metabotropic receptors to alter postsynaptic activity. Receptor type determines the speed and duration of the response.

Lesson 2 • Neurotransmitter Termination

Signal termination occurs via reuptake, enzymatic degradation, or diffusion. Efficient clearance prevents receptor overstimulation and resets the synapse.

Lesson 3 • Synaptic Integration

Postsynaptic neurons integrate multiple inputs to determine whether to fire. Integration rules link synaptic events to whole-neuron output decisions.

Lesson 4 • Synapse Structure and Types

Synapses are specialised junctions between neurons or between neurons and effectors. Structural knowledge underpins all transmission concepts in this chapter.

Lesson 1 • Gaseous and Unconventional Transmitters

Nitric oxide and endocannabinoids act as retrograde messengers, diffusing backward across synapses. Their mechanisms challenge classical transmission models.

Lesson 2 • Glutamate and GABA Systems

Glutamate is the primary excitatory transmitter; GABA is the primary inhibitory transmitter. Their balance governs overall brain excitability.

Lesson 3 • Monoamine Neurotransmitters

Dopamine, serotonin, norepinephrine, and histamine modulate mood, arousal, and reward. Their diffuse projections influence broad brain regions.

Lesson 4 • Neuropeptides and Neuromodulators

Neuropeptides act as slow, long-lasting modulators that fine-tune synaptic transmission. They complement fast transmitters by adjusting circuit gain.

Lesson 1 • Basic Circuit Motifs

Feedforward, feedback, and lateral inhibition are recurring circuit patterns. Recognising motifs allows prediction of circuit-level computations.

Lesson 2 • Oscillations and Rhythmic Activity

Neural oscillations arise from synchronised network activity and support cognition. Frequency bands correlate with distinct functional states.

Lesson 3 • Sensory Processing Circuits

Sensory systems transform physical stimuli into neural codes through layered circuits. Understanding these circuits links cellular events to perception.

Lesson 4 • Network-Level Computation

Networks perform computations such as pattern completion, winner-take-all selection, and gain control. These operations emerge from circuit architecture.

Lesson 1 • Hebbian Plasticity Principles

Hebb's rule states that co-active neurons strengthen their connections. This principle underlies associative learning at the synaptic level.

Lesson 2 • Long-Term Depression

LTD persistently weakens synapses and is essential for memory specificity and motor learning. It balances LTP to prevent runaway excitation.

Lesson 3 • Spike-Timing-Dependent Plasticity

STDP modifies synaptic strength based on the precise timing of pre- and postsynaptic spikes. It provides a biologically realistic learning rule.

Lesson 4 • Homeostatic and Structural Plasticity

Homeostatic plasticity stabilises neuronal activity by scaling synaptic strengths globally. Structural changes such as spine growth consolidate long-term memories.

Lesson 1 • Amygdala and Emotional Signalling

The amygdala assigns emotional salience and drives fear learning through defined circuits. Its outputs modulate memory, attention, and autonomic responses.

Lesson 2 • Hippocampal Memory Circuits

The hippocampus encodes episodic and spatial memories through trisynaptic and direct pathways. Its circuit organisation exemplifies plasticity in action.

Lesson 3 • Neuromodulation Across Brain States

Arousal systems broadcast neuromodulators that shift global brain state and cognitive mode. State-dependent signalling explains variability in neural responses.

Lesson 4 • Reward Circuitry and Dopamine

Dopaminergic neurons signal reward prediction errors to drive motivated behaviour. Understanding this circuit links neuron physiology to decision-making.

Lesson 1 • Neurodegenerative Disease Mechanisms

Protein aggregation, mitochondrial failure, and synaptic loss drive progressive neuron death. Mechanistic understanding guides biomarker and therapeutic development.

Lesson 2 • Channelopathies and Epilepsy

Mutations in ion channels alter excitability and can trigger seizure activity. Linking channel dysfunction to network hyperexcitability is clinically essential.

Lesson 3 • Psychiatric Disorders and Synapse Pathology

Schizophrenia, depression, and anxiety involve disrupted synaptic signalling and circuit connectivity. Neurotransmitter imbalances provide targets for pharmacological treatment.

Lesson 4 • Excitotoxicity and Neuronal Death

Excessive glutamate activation causes calcium overload and neuronal death. This mechanism underlies acute injuries such as stroke and traumatic brain injury.