Ch12 Learning and Memory

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35 Terms

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fixed action pattern

species-specific evolved pattern of complex behavior as a reponse to a specific stimulus

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habituation

occurs when an organism reduces its behavioral response to an unchanging, harmless stimuli

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sensitization

occurs when repeated exposure to a strong stimulus increases response to other similar environmental stimuli

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delay conditioning

type of classical conditioning when the CS overlaps with the UCS

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trace conditioning

type of classical conditioning when the CS and UCS do not overlap in training, requires conscious declarative processes

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extinction

in classical conditioning when exposure to the CS without the UCS reduces CRs (does not generalize outside of the training situation)

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long-term habituation

fewer presynaptic terminals of sensory neurons (signal does not get sensed as often)

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long-term sensitization

more presynaptic terminals of sensory neurons, more dendrites on motor neurons (sends signals more frequently)

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biochemical correlates of sensitization

  1. serotonin at axo-axonic synapse between interneuron and sensory neuron activates the enzyme adenyl cyclase

  2. adenyl cyclase converts ATP into messenger cAMP

  3. cAMP activates protein kinase A (PKA)

  4. PKA decreases K+ current, prolongs action potential, signals vesicles to move into release zone, and opens more CA2+ channels

all leads to enhanceed glutamate release from sensory neurons

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cAMP-PKA-MAPK-CREB pathway

leads to long-term changes in behavior and structural changes in sensory neurons

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amygdala in learning and memory

threat conditioning

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cerebellar circuits in classical conditioning

cerebellar granule cells provide info about the CS

climbing fibers from the medulla synapse on Purkinje cells, provide info about the UCS

Purkinje cells synapse on cells in interpositus nucleus

*learning occurs when climbing fibers(UCS) and parallel fibers (CS) synapse onto a Purkinje cell and fire at the same time*

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stages of memory

encoding → storage → retrieval

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atkinson-shiffrin multistore model of memory

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types of declarative memory

episodic (events) and semantic (facts)

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types of non-declarative memory

procedural, perceptual representation, classical conditioning, and nonassociative learning

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episodic memory in the brain

hippocampus

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semantic memory in the brain

cortex

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procedural memory in the brain

basal ganglia

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perceptual representation in the brain

sensory systems

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classical conditioning in the brain

cerebellum

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nonassociative learning in the brain

reflex pathways

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anterograde amnesia

inability to encode new memories

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retrograde amnesia

loss of past memories

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Hebb’s Law basics

neurons that fire together wire together

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long-term potentiation

??

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associative long-term potentiation (LTP) rules

cooperativity: inputs must be active at the same time

associativity: weak inputs are potentiated when fired with strong ones

specificity: only the stimulated synapse shows potentiation

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spacial mapping paradigms

hippocampus (dependent on): place cells, where am I?

subiculum: direction cells, where am I going?

entorhinal cortex: grid cells, what’s my environment?

*Morris water maze

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semantic memory networks

anterior temporal lobe is the “hub” of semantic cognition (part of language area)

ventral ATL: connects with core semantic areas

dorsal ATL: connects with language and auditory processing areas

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what does the striatum do

helps form procedural memory

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basal ganglia in memory

involved with memories of motor patterns

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nucleus accumbens in memory

emotional and reward correlates of procedures

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short term memory involves what area

frontal cortex, think object permanence in toddlers

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reactivation and reconsolidation

synapses are weakened when info is retrieved, retrieval stimulates same consolidation processes as the original learning.

reconsolidation updates memory to sometimes include ongoing current information at the time of retrieval, sometiems false info

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stress and memory

stress as alertnesswith learning immproves memory

stress produces a refractory period, causing a delay between stress and learning, which might impair memory