Learning and Memory: Core Definitions

Learning
A change in behaviour resulting from experience; involves acquiring new knowledge or skills.

Memory
The retention of learned information over time.

Types of Memory

Memory Type	Description	Brain Regions
Declarative (Explicit)	Conscious memory for facts and events	Medial temporal lobe, hippocampus
Non-declarative (Implicit)	Unconscious memory for skills, habits, priming, emotional learning	Cerebellum, striatum, amygdala

Categories of Learning

Learning Type	Subtypes	Description
Non-associative	Habituation, Sensitisation	Changes in response to a single repeated stimulus
Associative	Classical Conditioning, Operant Conditioning	Learning relationships between stimuli or between behaviour and outcomes

Memory Duration and Consolidation

Stage	Duration	Properties
Short-Term Memory	Seconds to hours	Fragile, easily disrupted
Long-Term Memory	Days to years	Stable, requires consolidation

Consolidation Processes

• Repetition and spaced practice
• Emotional engagement
• Active encoding
• Structural changes at synapses (LTP/LTD)

Structural Changes and Neuroplasticity

Neuroplasticity
The brain’s ability to reorganise circuits in response to experience.

Neurogenesis
Formation of new neurons, particularly in the hippocampal dentate gyrus.

Factors Affecting Neurogenesis

Factor	Effect
Exercise	Increases neurogenesis; improves learning and memory
Depression	Reduces hippocampal neurogenesis
Antidepressants	Enhance neurogenesis
Enriched environments	Increase dendritic branching and synaptic strength

Synaptic Pruning and Neuronal Death

• Neurons compete for growth factors; those failing to connect die.
• Unused synapses and dendrites are removed.
• “Use it or lose it” applies to neural structure.

Experience-Driven Reorganisation

• Musicians: enlarged somatosensory/motor maps.
• Therapy (e.g., CBT): measurable changes in neural activation patterns.

Synaptic Plasticity

Synaptic plasticity refers to long-lasting changes in synaptic strength, forming the basis of learning and memory.

Long-Term Potentiation (LTP) and Long-Term Depression (LTD)

Property	LTP (High-Frequency Input)	LTD (Low-Frequency Input)
Effect	Strengthens synapse	Weakens synapse
Ca²⁺ level	Large influx	Small influx
Enzymes	Kinases (CaMKII, PKC)	Phosphatases
AMPA receptors	Inserted/increased sensitivity	Removed/internalised

Hebbian Rule

“Neurons that fire together, wire together.”

Properties of LTP

Property	Meaning
Specificity	Only active synapses strengthen
Co-operativity	Stronger effects when inputs activate together
Associativity	Weak input strengthened when paired with strong input

Role of NMDA Receptors

• NMDA receptors are normally blocked by Mg²⁺.
• Depolarisation removes Mg²⁺ → Ca²⁺ enters → triggers LTP cascade.
• Blocking NMDA receptors leads to impaired learning (e.g., Morris water maze deficits).

Working Memory and the Hippocampus

Working Memory
Short-term storage and manipulation; located in the prefrontal cortex.
Assessed with delayed-response tasks.

Effects of Hippocampal Damage

Deficit	Description
Anterograde amnesia	Inability to form new memories
Retrograde amnesia	Loss of recent past memories
Declarative memory impairment	Facts and events affected
Procedural memory intact	Skills preserved (e.g., Patient H.M.)

Tasks Assessing Hippocampal Function

• Object recognition
• Radial arm maze
• Morris water maze
• Delayed matching-to-sample

Memory Loss in Alzheimer’s Disease

Symptoms

• Progressive memory loss
• Personality and behavioural changes
• Cognitive decline
• Apraxia (motor difficulty)
• Aphasia (language impairment)
• Agnosia (difficulty recognising stimuli)

Neurochemical Basis

• Significant reduction in acetylcholine (ACh) in the hippocampus, cortex, and striatum.

Treatments

• Cholinergic drugs that increase ACh availability or mimic ACh.
• Provide temporary, modest improvements in memory.