13. Experience dependent plasticity PDF

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Summary

The Basic Principles of Associative Learning: not necessary but variables Leaning through reinforcements (usually for instrumental but also through pavlovian) - Association by Contiguity: - Co-occurrence in space and time (Lil contiguity b/w taste and illness) Arbitrariness : Any stimulus, any respo...

Description

The Basic Principles of Associative Learning: not necessary but variables -

Leaning through reinforcements (usually for instrumental but also through pavlovian)

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Association by Contiguity:

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Arbitrariness:

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Empty Organism

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Co-occurrence in space and time Any stimulus, any response

(Lil contiguity b/w taste and illness) (No learning b/w CS and shock or noise/light and illness)

Organism is a black box -> You are the sum of your associations (Certain associations are easier established than others)

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Passive organism

- aka Preparedness Principle -> Seligman 1970

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Learning happens to you

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You cannot control what you are reinforced or what you have learned.

Taste Aversion Learning/ Bait shyness Garcia and Koelling (1966) -

Compound Conditioned stimulus (CS) -

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Bright, noisy (click) and sweetened water. -> conditioned stimulus w/ diff parts

2 subgroups -

Group 1 when licked => Mild footshock (immediate discomfort) -> aversive conditioning

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Group 2 when licked => X-rays (delayed illness)

Test = choice between flavored water or the bright (light) water w/ clicking noise. -

Group 1 = perfect contiguity (bright, noisy and sweet all happen at the same place and time) -

Group 1 should avoid bottles bc/ all 3 components were paired w/ foot shock (afraid of that bottle (Bottle A))

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Group 2 = low contiguity bc/ it had a delayed response (nausea) to the x ray (which it associates w/ the water) -

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Group 2 should avoid one or none of these bc poor contiguity.

Basic principles of conditioning aren't necessary for conditioning

Results: Subjects that were made ill, avoided the sweet water, but those that received shock, avoided bright/noisy water -

Group 1 = Foot shock -> not related to internal states (ex. Flavor) so fear is of external traits (ex. Light and noise)

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Group 2 = Illness -> internal state (flavor)

What about the idea of reinforcement? Edward Tolman’s Latent Learning Effect: do we need reinforcement? 3 conditions -

Group 1 : never reinforced through the maze -

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Group 2 : Always reinforced -

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Still made many ‘mistakes’

V fast to learn the path and get there

Group 3 : Reinforced after 10 days -

Learned the path in 2 trials bc actually wants to get there

Latent learning

Reinforcement is needed to ‘show learning’

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Learning that is occurring but we’re not seeing it

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Group 1 and 3 was learning but only group 3 had incentive to follow that path.

Taxonomies of Memory Associative versus non-associative Learning and Memory

1. Non-associative learning learning based on repeated experience with a stimulus. stimulus memories -

Habituation -> decreases in effect.

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Sensitization -> increases in effect.

2. Associative learning

1. Declarative (Explicit) Semantic - Factual knowledge about the Episodic - Events, Autobiographical

2. Non-Declarative (Implicit)

learning relationships between

- Procedural *if/then memories

stimuli, behaviours and/or events

- Skill learning, conditioning, non-associative

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Respondent (type 1) conditioning.

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Operant (type 2) conditioning.

Search for the Memory ‘Engram’ Karl Spencer Lashley Research Question: When have rats that learn to navigate a maze, where in the brain is this information stored? -

Let the rat learn the maze,

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Systematically damage parts (created small lesions) of the brain-focused solely on the cortex. -

Discrete (small) lesions of cortical areas did not interfere with maze learning, but large areas of damage did.

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As the percentage of lesion increased, so did the number of errors that the rat had in escaping the maze.

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Deficit in memory was proportional to the amount of damage produced in the cortex. -

Not the particular place in the cortex that affected memory, but the amount

“This series of experiments has yielded a good bit of information about what memory is not. It has discovered nothing directly of the real nature of the ‘engram’. I sometimes feel, in reviewing the evidence… that the necessary conclusion is that learning is not possible” - (K. Lashley, 1950). -

Lashley argued : “if no particular part of the brain responsible for learning -> learning must not be possible”

Principle of Equipotentiality All cortical regions can mediate learning equally

Principle of Mass Action Ability to learn is proportional to the amount of cortex available.

Subcortical Areas Involved in Learning and Memory: Hippocampus and Amygdala Certain areas of the brain are involved in certain types of learning and memory.

Dedicated Memory Storage Areas of the Brain Hippocampus => declarative and spatial memories -

(e.g. case of H.M. removed proportions of his hippocampus and amygdala and he had a profound form of amnesia. He could also not form new memories)

Cerebellum => procedural memories (simple Pavlovian associations) -

HM would get better at procedural tasks but not remember

Amygdala => emotional memories (Pavlovian associations) -

Emotions but not just

Frontal Cortex short-term/working memory

How are memories stored? Synaptic Basis of Learning and Memory Pavlov’s Cortical Model : Ur brain creates a physical connection formation of (psychological) associations (CS-US) creates new cortical connection.

Golgi technique or Silver Stain : Wire-like things in brain (Ramón y Cajal, 1852 - 1934) Golgi technique used to examine neurons under a microscope. -> drew the neural systems

Cellular Basis of Memory Neurogenesis Creating Novel Circuits -

OLD: prior to the mid-1990s.

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NEW: neurogenesis does occur in the mammalian brain.

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The mammalian brain doesn’t make new neurons in adulthood.

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Olfactory bulb, hippocampal formation, and possibly the neocortex.

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Reason for neurogenesis is still unclear

Environmental Experiences Alters Brain Morphology A type of experience that causes neurogenesis Raising rats in enriched (social, w/ toys etc) enclosures increases: -

Brain weight -> change in structural brain

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Dendritic length and complexity - ‘Sholl analysis’ (long = complex nervous system)

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Enhanced vascular volume - (more blood vessels)

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How many branches come off dendrite?/how many circles does dendrite cross?) Cells need oxygen and glucose through the blood

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Number of synapses per neuron (synaptic spine counting) (Johansson and belichenko, 2002)

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Mitochondrial volume (marker of greater metabolic activity)

Structural Basis of Memory Cajal proposed that structure/morphological changes store memories, -

e.g. the formation of new synapses, growth of dendritic processes (branches and spines)

What does this have to do with memory? Cellular Basis of Memory-Synaptic Basis of Memory -

New synapses could be generated to store specific new memories.

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Existing synapses could be modified to store the memories.

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A pool of new synapses could be continuously generated, -

Learning and memory incorporates them into a functional storage network. (stabilizes the network)

Donald Hebb 1904 - 1985 -

New synapses are continuously generated in the brain.

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New synapses are anatomically and physiologically connected, but not part of a memory network.

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Upon appropriate activation – synapses are “strengthened” and incorporated into a memory network.

Cellular Basis of Memories “Hebbian Synapse” “When an axon of a cell A (presynaptic cell) is near enough to excite a cell B (post-synaptic cell) and repeatedly or persistently take part in firing it, some growth process or metabolic change takes place in one or both cells that A and/or Bs efficacy (ability to fire) is increased” - In 1949, Donald Hebb Key points -

Simultaneous pre-and post synaptic activity

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Some sort of change in the connection between the neurons

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Increase in the influence hat pre synaptic neuron has over postsynaptic activity AKA :

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1 cell fires (1 black circle) -> post synaptic cell does not fire

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2 cells fires (both black circles) -> post synaptic cell does fire -

Now, there is a change in the presynaptic or postsynaptic cell (red circle)

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Next time, 1 cell fire (red cell on top) is enough to make it that postsynaptic does fire

Whole cell- electrophysiology -

Allows us to actually see the electrical activity (stimulate individual cells/ listen to other cells)

First evidence for hebbian learning and memory Habituation = learned suppression of a response to a repeated stimulus Eric kandel -> studied appalachian sea snails -

If u stimulate the snail siphon, the snail withdraws its gill for protections -

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This is cause it activates the motor neuron that withdraws the gill

Repeated stimulation => stimulus leads to a decrease in neurotransmitter release into the synapse and thus motor neuron -

The stimulation causes the snail siphon to not work as well. This is cause of habituation, gets used to the electrical response thus its a learned suppression of the release of neurotransmitter into synapse.

Long term potentiation (LTP)...