Chapter 12: Learning and Memory: Basic Mechanisms
Lecture Outline
Learning Paradigms
Synaptic Plasticity
Perceptual Learning
Classical Conditioning
Reinforcement
Learning
"...relatively permanent changes in behavior produced by experience"
Learning involves changes in the nervous system
Physical/chemical
Learning allows us to tailor our behaviors to the environment: allows for adaptation
Learning involves the motor, sensory, and memory systems
Forms of Learning
Perceptual: identify objects and situations
Stimulus-Response: connections between stimuli and motor responses
Classical conditioning
Operant Conditioning
Motor: form new circuits in motor system
Relational: identify connections between stimuli
Classical Conditioning
Involves making connections between two forms of stimuli:
Unconditional (US): reliably provokes a response
Response is termed unconditional (UCR)
Conditional (CS): neutral: does not provoke the response
Pair the CS and UCS over many trials
Does the CS alone produce a response?
The Hebb Rule
Hebb argued that synapses that are active at the same time that the postsynaptic neuron fires are strengthened over time
Implies physical changes in the nervous system
Rosensweig: enriched environment studies
Noted specific changes in brains of enriched rats
Thicker cortex
More glial cells
More Ache (perhaps more ACh?)
Long-Term Potentiation
Cells in entorhinal cortex project via perforant path to synapse onto granule cells in the dentate gyrus
LTP procedure: electrically stimulate perforant path (100 pulses/over a few seconds)
Then observe postsynaptic potential induced by a single pulse given repeatedly over days
LTP is indexed by gradual increase in PSP size
Diagram of the LTP Procedure
Long-Term Potentiation
LTP requires:
Activation of synapses and depolarization of postsynaptic membrane
LTP involves
Release of glutamate
Activation of NMDA receptors in depolarized membrane
Entry of calcium ions
Mechanisms of LTP
LTP may result from :
Increased release of transmitter
Increased number of receptors
Greater linkage of receptors to ion channel openings
Increased number of synapses
Other causes?
A Biochemical Model of LTP
Glutamate release
NMDA receptors
Non-NMDA rec.
Calcium entry
NO feedback onto presynaptic cell
Perceptual Learning
Learning about simple perceptual objects occurs in association cortex:
Visual perceptual learning
Ventral stream: "what" object issues
Ability to differentiate visual patterns requires intact connections between visual cortex and inferior temporal cortex
Dorsal stream: "where" object issues
PET studies: document ventral/dorsal stream activation during object- and spatial-memory tasks
Role of ACh in Learning and Memory
Deutsch: noted that anticholinergic drugs impair learning in animals and humans
Alzheimer’s disease involves memory loss
Damage to ACh cells in Alzheimer’s disease
Nuc. Basalis--> neocortex
Medial septum--> hippocampus
Footshock induces ACh release in auditory cortex: sharpens tone detection
Classical Conditioning
Footshock (FS) : activates cells in basolateral amygdala--> activates central amygdala
Central amygdala--> freezing, autonomic changes
Tone: activates cells in the medial geniculate
CER learning: Tones paired with FS come to elicit freezing
May be due to LTP-like processes in thalamus, amygdala
CER is blocked by AP5 (NMDA antagonist) in amygdala
Reinforcement
Olds and Milner study:
Electrical stimulation of rat brain induces reinforcement
Responses that produce brain stimulation are repeated (e.g. bar press, alley running)
Dopamine plays a critical role in self-stimulation
Mesolimbic dopamine system
Ventral tegmentum to accumbens, amygdala, septum
Mesocortical dopamine system
Nuc. Accumbens and Reinforcement
Self-stimulation is supported by electrodes placed along mesolimbic path
Rats will self-inject dopamine agonists directly into the nuc. accumbens
Natural reinforcers increase extracellular dopamine levels in nuc. accumbens
Microdialysis studies
Drugs of abuse also increase DA release
DA and Motivated Behaviors
Natural and conditioned reinforcers may act via stimulating DA release in the nuc. accumbens
Conditioned punishers may reduce DA in nuc. accumbens
Mark et al (1989): after CTA learning, saccharin taste reduces DA level in nuc. accumbens
Relational Learning and Amnesia
Human Anterograde Amnesia
Retrograde vs. anterograde amnesia
Hippocampal damage
Declarative Memory
Relational Learning in Animals
Working memory
Spatial learning
Cholinergic function and memory
Amnesia
Amnesia: failure to remember
Anterograde: amnesia for events that occur after a trauma
Retrograde: amnesia for events that occur prior to the trauma
Amnesia can be
Temporary: e.g. minor concussion
Permanent: focal brain damage
Korsakoff’s Syndrome
Associated with chronic alcoholism
Thiamine deficiency produces brain damage
Effects include:
Severe anterograde amnesia
Confabulation: person unknowingly creates fictitious memories
Hippocampal Damage in Humans
Anterograde amnesia follows bilateral damage to the hippocampus
Patient H.M. suffered from severe epilepsy
Therapy in 1953 was to remove medial temporal lobe (including the hippocampus)
H.M. showed severe anterograde amnesia
No retention for events since 1953
Can recall events prior to 1953
Amnesia was localized to hippocampus
Memory Processing
Short-term Memory (STM)
Limited capacity (7 items)
Brief duration
Can be lost without rehearsal
Long-term Memory (LTM): permanent storage
Consolidation: Process by which rehearsal of information in STM results in transfer to LTM
Learning/Memory Capabilities of Patient H.M.
Patient H.M. exhibits:
Severe anterograde amnesia
Normal STM
Normal LTM for events prior to the surgery
Normal perceptual learning
Normal sensory-response learning
Normal motor learning
H.M.’s problem is transfer from STM to LTM
Memory Processes
Declarative memory: memories available as facts, events, or specific stimuli
Where I parked my car this morning
Nondeclarative memory: stimulus-response and motor memories that control behaviors at an unconscious level
How I drove my car to work this morning
Hippocampal Anatomy
Inputs of hippocampus
Entorhinal cortex gets input from amygdala, all association areas of cortex
Fornix
Outputs of hippocampus
From field CA1 and subiculum to entorhinal and association cortex
Anterograde Amnesia after Hippocampal Damage
Patient R.B.
Suffered heart attack- reduced blood flow to brain
Later developed permanent anterograde amnesia (AA)
Histological examination of his brain (post-mortem) showed:
Loss of cells in field CA1 of the hippocampus
Monkey/rats studies:
Anoxia results in damage to field CA1 and AA
Relational Learning in Animals
Relational learning is impaired in animals after hippocampal damage
Olton’s radial maze studies: food placed in maze arms
Intact rats remember arms that were visited earlier
Rats with hippocampal damage are unable to recall the arms have been visited previously
Hippocampal damage reduces recall of events that occurred earlier that day (time relations)
Spatial Perception After Hippocampal Damage
Navigation requires recall of spatial landmarks that guide our movements
Morris water maze: rats must find platform submerged under cloudy water
Normal rats are able to learn the position of the platform regardless of where they are placed in maze
Hippocampal rats cannot learn this relational problem
Hippocampal damage disrupts navigation in homing pigeons...
Cholinergic Modulation of Hippocampal Function
ACh: involved in theta rhythms of hippocampus
Antagonism of ACh: disrupts spatial working memory
ACh transplants into rat brain can reverse effects associated with fornix damage
ACH agonism can reverse effects associated with diminished cholinergic function