Learning and Memory

What is Learning and Memory?

  • Learning: Acquisition of information that alters future behavior, improving adaptive behavior, modifying actions to increase survival (e.g., finding food/water or avoiding danger).

  • Memory: Retention of learned information, crucial for future behavior.

Principles of Learning:
Associative Learning

  • Classical Conditioning:

    • Unconditioned Stimulus (US): Naturally evokes a response without prior training.

    • Unconditioned Response (UR): Natural response to an unconditioned stimulus.

    • Conditioned Stimulus (CS): Initially neutral cue paired with US, eventually elicits a response.

    • Conditioned Response (CR): Trained response to CS predicting US.

  • Example:

    • Before training: Bell (CS) → No response.

    • During training: Bell (CS) + Food (US) → Salivation (UR).

    • After training: Bell (CS) → Salivation (CR).

Extinguishing an Old Association

  • Extinction: Process of reducing a learned response by ceasing to pair the stimulus with reinforcement. This involves both unlearning and forming new opposing responses.

Leon Kamin’s Blocking Effect (1969)

  • Blocking: Prior training on one cue (CS1 → US) prevents learning of a second cue (CS2) when both are paired together (CS1 + CS2 → US).[

  • Example: Pre-trained rats (light CS = shock US), then exposed to tone + light CS, result in not learning that tone also associate with shock [learning was blocked]

Learning Prediction and Error

  • Surprise: Memory improves with surprise. Greater surprise leads to stronger learning due to prediction error.

  • Prediction Error: Difference between an expectation of the US (reward/shock) and the actual outcome.

  • Error-correction learning: Mathematical detail of conditions for learning based on the degree of surprise.

  • Rescorla-Wagner Rule: Changes in CS–US associations driven by prediction error;

Neurobiology of Prediction Error

  • Monkeys: Electrophysiological recordings show reduced firing in neurons when there is no reward indicating prediction error.

    • other studies with rats and monkey suggest that the orbitofrontal cortex is also responsible for expectation and error signaling

  • Humans: Dopaminergic cells activate with prediction errors, with increased activity in the nucleus accumbens during unpredicted rewards.

Animal and Patient Studies on Fear learning

  • Following brain lesions: Animal studies demonstrate amygdala lesions (from muscimol injection before conditioning or before testing) impair fear conditioning.

    • Case of Urbach-Wiethe Disease: Bilateral amygdala degeneration leads to impaired fear learning.

Memory

  • Types of Memory:

    • Episodic Memory: experiences. [explicit] - hippocampus

    • Semantic Memory: Facts [explicit] - perirhinal cortex

    • Procedural Memory: Skills [implicit] - prefrontal cortex(through motor cortical reigions and subcortical areas) + cerebellum (coordinating, motor sequence)

Perceptual Memory: Stages of Visual Memory

  1. Sensory Memory: e.g., “Iconic” memory lasts < 1 second (Sperling's Task [tone and row of letter recall]).

  2. Short-term Memory: <1 minute. Linked with working memory; evidence shows sustained neural activity occurs in the inferotemporal cortex.

    • fMRI evidence: 1. Activity in the temporal visual association cortex that is sustained beyond visual stimulus presentation. 2. Activity in higher temporal areas is more persistent than in occipital areas earlier on in the visual pathway

    • TMS evidence: disrupted visual association cortex = impair short-term memory performance

  3. Long-term Memory: Lasts a lifetime includes explicit and implicit; can be studied via object recognition tasks.

    • Behavioral Evidence: Damage to certain cortical areas impairs long-term retention.

    • Animal evidence:

      • Electrophysiology recordings: reduced response in IT to complex stimulus

      • Brain lesion: damage to perirhinal and parahippocampal cortices was done to tasks that require 24hr retention of visual discrimination memory

    • Human evidence:

      • fMRI: repetition suppression effects were observed in visual association cortical areas (as well as prefrontal areas)

      • Brain lesion: lesion to temporal lobe [perirhinal and parahippocampal cortices]= amnesia

Important Case Studies

  • Case of H.M.: Underwent hippocampus and amygdala removal; suffered profound anterograde amnesia (can’t form new memories) and minor retrograde amnesia (can’t remember past experiences before the treatment) but retained some intellectual functions (improved IQ).

  • Case of K.C.: Damage to hippocampus led to episodic memory loss, but semantic memory remained intact.

  • Semantic Dementia Patient: Inability to recognize familiar objects or obj that was just shown to them due to perirhinal cortex damage.

Hippocampus & spatial navigation

  • Damage to hippocampus = impair spatial navigation

  • Experiment: Group1: randomly assigned starting point vs Control group: just follow arrows

    • Found: hippocampus activated more in group1

  • Accuracy of the path adopted correlated with the level of activity in the hippocampus

  • Animal Experiment: spatial water maze (rats and cloudy water)

    • Found: lesion in hippo disrupts performance in water maze, and success in navigation activates gene expression in hippo

Memory Consolidation

  • Consolidation Process: Transforms fragile new memories into stable ones through synaptic and systems consolidation.

    • Synaptic (Cellular) Consolidation: Rapid changes at synapses; occurs minutes to hours.

    • Systems Consolidation: Gradual neural circuits reorganization; spans months to years.

    • occurs together at different speed

Synaptic plasticity (Donald Hebb 1949)

  • SP is the ability to adapt the neural connection; synaptic connection btw 2 neurons is strengthen by learning

  • Long-term potentiation (LTP): a persistent strengthening of synaptic connections in the brain, resulting in a long-lasting increase in signal transmission between neurons

    • If one of the pathways into the hippo was stimulated at a high frequency, the subsequent response to the stimulation would increase

    • Associated LTP: LTP that depends on co-activation of 2 inputs (underpinning associative learning)

    • Non-associated LTP: induced activity in a single input pathway

System consolidation

  1. Standard Theory: Suggests old memories may not require the hippocampus as they consolidate

    • Some old memories remain intact (there is temporal gradient in retrograde amnesia)

    • Transfer of dependence of old memories to the cortex

    • hippocampus is believed to be only essential at first because we needed to retrieve it but after cortical areas are linked the memories stay and hippo is not needed anymore.

  2. Multiple Trace Theory: memory retrieval creates new traces; all episodic memories might depend on the hippocampus to some extent.

    • No old memories remain intact (flat retrograde amnesia)

    • Hippocampus is usually only partially damaged

    • The more traces the greater chance that some memories remain intact due to partial hippocampal damage

    • Meaning partial hippo damage sometimes lead to flat retro amnesia while sometimes lead to gradient retro amnesia