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Classical conditioning
Ivan Pavlov
Involves linking two stimuli to alter the reaction to one.
Stimuli types
Conditioned stimulus: A neutral stimulus that, after repetition, elicits a response. (CS)
Unconditioned stimulus: A stimulus that automatically elicits a response. (UCS)
Operant (Instrumental) Conditioning
Learning based on consequences.
Reinforcement: Rewards that increase the likelihood of a response.
Punishment: Consequences that decrease the likelihood of a response.
Engram
Physical trace of a learned experience.
Lashley’s Engram Early hypothesis
Cutting the connection between brain regions should erase the new learning. (disproven)
Lashley’s principles
Equipotentiality: Every part of the cortex contributes equally to complex behaviors.
Mass Action: The entire cortex works together; more cortex results in better performance.
Engram modern research (Thompson)
Proposed classical conditioning engram is in the cerebellum, specifically lateral interpositus nucleus (LIP), not the cortex.
Findings of modern research (engram)
Lateral interpositus nucleus (LIP) is crucial for learning.
Responses in LIP increase as learning occurs.
Concluded from experiments that learning happens in the LIP.
Identified specific cells and neurotransmitters involved in changes in the LIP.
Results from PET Scans on Young Adults (Engram)
Revealed the cerebellum is crucial for classical conditioning.
Only when the delay between the conditioned stimulus (CS) and unconditioned stimulus (UCS) is short.
Types of memory
Short-term Memory (STM): Memory of recent events with limited capacity that fades quickly without rehearsal.
Long-term Memory (LTM): Memory of past events with unlimited capacity that persists over time and can be stimulated with cues.
Memory Process
Information first enters short-term memory. Brain consolidates some information into long-term memory.
Findings:
Distinction between short and long-term memory is less clear.
Not all rehearsed short-term memories become long-term.
Emotionally Significant Memories
Epinephrine and cortisol boost the consolidation of recent experiences.
Emotional experiences → Locus coeruleus → Norepinephrine → Cortex & dopamine → Hippocampus.
Working memory
A temporary storage system for actively manipulating information, primarily stored in the prefrontal cortex.
Findings:
Prefrontal cortex stores this information.
Damage to this area affects performance and impairment can be very specific.
Delayed responce
Common working memory test. Involves responding to recently seen or heard information.
Prefrontal Cortex Activity in working memory
Declining activity in the elderly is linked to decreasing memory.
Increased activity suggests compensation for other brain regions.
Hippocampus
Crucial for forming new long-term and episodic memories, as well as spatial and contextual navigation.
Various areas are active during memory formation and recall.
Damage = amnesia.
Amnesia
Memory loss.
Anterograde: Inability to form new long-term memories.
Retrograde: Loss of older memories from before brain damage.
Explicit memory (declarative)
Conscious recall of information or facts.
Procedural Memory
A type of implicit memory involving motor skills and habits.
Implicit memory
Influence of past experiences on behavior without conscious awareness.
Memory loss
Difficulty imagining future events due to the inability to use past experiences.
Brain damage types
Korsakoff’s Syndrome
Alzheimer’s Disease
Korsakoff’s Syndrome
Memory loss caused by thiamine (Vitamin B1) deficiency, often due to chronic alcoholism; patients may confabulate (fill gaps with false info).
Leads to memory loss, especially for recent events.
Effect: Impairs the ability to metabolize glucose. Leads to neuron loss or shrinkage.
Symptoms of Korsakoff’s Syndrome
Confabulation: Making guesses or stories to fill memory gaps.
Apathy: Lack of motivation or interest.
Confusion: Disorientation in time or place.
Memory loss: Difficulty forming new memories and recalling recent events.
Alzheimer’s Disease
Progressive memory decline linked to the build-up of Amyloid Beta (forming plaques) and Tau (forming tangles) proteins.
Caused by degeneration of brain cells.
Begins with difficulty remembering new information and impacts daily functioning.
Alzheimer’s Disease components
Amyloid Beta Protein: Causes widespread damage to the cerebral cortex, hippocampus.
Tau Protein: An abnormal form affects the support system inside neurons.
Plaques: Formed from damaged axons and dendrites.
Tangles: Formed from degeneration within neurons.
Theories on function of hippocampus
Hippocampus Function Research
Delayed Matching-to-Sample Tasks
Delayed Non-Matching-to-Sample Tasks
Hippocampus Function Research
Essential for declarative memory (episodic memory).
Research with Rats: Damage affects performance on two types of tasks.
Delayed Matching-to-Sample Tasks
Rat sees an object. Later, it must choose the matching object.
Delayed Non-Matching-to-Sample Tasks
Rat sees an object. Later, it must choose a different object from the sample.
Hippocampus & Spatial Memory
Hippocampus Damage
Radial waves
Morris Water Maze
Hippocampus Damage
Affects spatial tasks; ability to remember locations and navigate spaces.
Radial waves
Navigate a maze with eight or more paths. Reward at the end of each path.
Morris Water Maze
Swim through murky water. Find a platform just under the surface.
Hippocampus & contextual memory
Hippocampus Hypothesis
Hippocampus role
Episodic memory
Hippocampus Hypothesis
Important for memory context, the “where,” “when,” and “how” of an experience.
Hippocampus role
Acts as a coordinator, reconstructing context.
Episodic memory
Recent memories: include detailed context..
Older memories: have less detail.
Storing information in the nervous system
Brain Activity and Memory:
Brain activity creates physical changes.
Not all changes are specific memories.
Memory storage
Memory Storage
Understanding how the brain stores memories is challenging.
Hebbian Synapse
A synapse that becomes more effective when the presynaptic and postsynaptic neurons are active together.
Long term Potentiation (LTP)
Process involving glutamate receptors (AMPA & NMDA) where repeated excitation leads to long-lasting increases in signal transmission between neurons.
When one or more axons repeatedly stimulate a dendrite, making the synapse stronger and more responsive.
Principles of LTP
Principles:
Specificity: Only highly active synapses get stronger.
Cooperativity: Two or more axons stimulating together create stronger LTP than one axon alone.
Associativity: Pairing a weak input with a strong input boosts later responses to the weak input.
Compensatory process
Synapses strengthen through learning (LTP), less-used synapses weaken to balance the system.
Mechanism:Depolarization removes magnesium blocking NMDA receptors, allowing calcium to enter the neuron and strengthen the synapse.
The LTP Process in Hippocampal Neurons
Repeated Glutamate Excitation
Magnesium Displacement
NMDA Receptor Activation
Repeated Glutamate Excitation
Activates AMPA receptors. Causes membrane depolarization.
Magnesium Displacement
Depolarization removes magnesium blocking NMDA receptors.
NMDA Receptor Activation
Glutamate excites NMDA receptors. Opens a channel for calcium ions to enter the neuron.
Long-Term Potentiation Effects
Increased activity in the presynaptic neuron.
Increased responsiveness in the postsynaptic neuron.
LTP significance
Understanding LTP is a step towards understanding learning.
Could lead to memory-improving drugs.
Learning enhancement:
Caffeine and Ritalin: Boost learning by increasing arousal.
Herbal Effects: Effects are uncertain for Ginkgo biloba, Bacopa monnieri.
Improving memory
Altering Gene Expression:
Scientists can change genes in mice to try to improve memory.
Effects: Some memory types slightly improve. But other types of memory can get worse, showing a trade-off.
Behavioral Methods:
Best way to improve memory is through practice and learning strategies. Supported by studies in both animals and humans.