S2 Neuro Exam 5: Learning And Memory

Front 1

4 sequential steps in memory

Back 1

1. encoding
2. consolidation
3. storage
4. retrieval

Front 2

Describe encoding

Back 2

newly learned info integrated w prior knowledge

Front 3

Describe consolidation

Back 3

encoded info converted into a form that can be permanently stored.
Associated with structural changes in the brain

Front 4

Describe storage

Back 4

actual deposition of memory into final location

Front 5

Describe retrieval

Back 5

accessing stored memory

-subject to distortion. dependent on working memory

Front 6

2 Primary classifications of memory are associated w/ diff circuitries. What are they?

Back 6

1. declarative (explicit) memory
-available to consciounsness
-expressed by language (telephone number, etc)
2. nondeclarative (implicit) memory
-cannot be retrieved consciously (riding a bike, etc)

Front 7

2 types of declarative (explicit) memory

Back 7

1. semantic
-knowledge of objects, facts, concepts
-words & their meanings
2. episodic
-events

Front 8

What neural circuitry is assoc w/ Declarative memory

Back 8

1. encoding: sensory systems via association cortices
2. consolidation: hippocampus & surrounding areas (temporal lobe)
3. storage: association cortex
4. retrieval: brain regions involved in sensory percept

Front 9

What lesions would create declarative memory deficits?

Back 9

medial temporal lobe lesions

(usually bilateral to notice symptoms)

Front 10

What would medial temporal lobe lesions cause?

Back 10

inability to consolidate info into long term memory

Front 11

____________ lesion would cause a greater deficit in memory for spatial representation

Back 11

right hippocampal


(declarative memory deficit)

Front 12

___________ lesion would cause greater deficits in memory for words, objects or people

Back 12

left hippocampal


(declarative memory deficit)

Front 13

__________ lesions would cause greater deficits in memory storage for object recognition

Back 13

surrounding cortices


(declarative memory deficit)

Front 14

_______________ degeneration due to Alzheimers is associated w/ loss of short term declarative memory

Back 14

Entorhinal cortex
(CA 1 area)

Front 15

________________, _________, & __________ degeneration due to Korsakoff syndrome (prolonged thiamine defic, alcoholics) is assoc. w/ loss of short & long term declarative memory

Back 15

hippocampal formation, mammillary bodies, & thalamus

Front 16

4 types of non-declarative (implicit) memory

Back 16

1. priming cues
2. procedural
-skills & habits
-sensory-motor adaption
3. associative learning classical & operant condition
- skeletal musculatural
- emotional response
4. non-associative learning habituation & sensitization

Front 17

T/F
Non-declarative memory circuitry involves the temporal lobe & midline thalamic nuclei

Back 17

FALSE

involves basal ganglia, prefrontal cortex, amygdala, sensory assoc cortex, cerebellum, & reflex pathways

Front 18

2 forms of associative learning (non-declarative)

Back 18

1. Classical (Pavlov) conditioning
-learning relationship btwn 2 stimuli
(fear involves amygdala)
(eye blink involves cerebellum)
2. Operant conditioning
-relationship btwn behavior & reward/punishment (involves nucleus accumens)
(food aversion, trial & error, addictive behaviors)

Front 19

2 forms of non-associative learning (non-declarative)

Back 19

*both involve one stimuli
1. habituation- repeated (harmless) stimulation decreases response
2. sensitization- repeated (harmfull) stimulation increases response
*responses involve sensory & motor pathways involved in motor reflex

Front 20

What is the amygdala involved in?

Back 20

association of sensory input (via cortex/subcortical) & emotional ouput (via HPT axis & autonomics)

*also has output responsible for emotional arousal to modulate memory processing (PTSD)

Front 21

Procedural memory is composed of 2 subsystems. One involves the striatum & is assoc w/ ___________

Back 21

habit & skill

*dorsal striatum (basal ganglia) required for learning skilled movement sequences (loops, tonic activity, etc)

Front 22

The second subsystem of procedural memory involves the cerebellum & mediates ______________

Back 22

sensory-motor adaptations

(ex: vestibulo-ocular adaptions)

Front 23

Damage to the _____________, Huntingtons, Parkinsons, are accompanied by inability to learn motor skills

Back 23

basal ganglia

(non-declarative memory damge)

Front 24

Damage to the ___________leads to failure to develop fear conditioning

Back 24

amygdala

(non-declarative memory damage)

Front 25

_____________ damage can also interfere w/ conditioned reflex learning (eye-blink reflex)

Back 25

cerebellum

(non-declarative memory damage)

Front 26

The process of converting working (short term) memory to long term memory is _____________

Back 26

consolidation

(inability to convert diff types of memory= forgetting)

Front 27

What areas are assoc w/ working (short term) memory

Back 27

hippocampus
prefrontal cortex & neocortical areas (more complex tasks of working memory, problem solving, etc)

Front 28

Declarative long term memory:
Semantic (factual) knowledge is stored in a distributed fashion in the __________.

Back 28

neocortex


(Damage to a specific area can lead to loss of specific info & fragmentation of knowledge (agnosia))

Front 29

Declarative long term memory:
Episodic (autobiographical) knowledge about time & place involves the ___________

Back 29

prefrontal cortex


(Frontal lobe damage assoc/ w tendency to forget how info was acquired (amnesia))

Front 30

Non-declarative long term memory:
For habituation/sensitization, fear cond., reflex, etc cortical storage is NOT required. Learning is supported by what structures?

Back 30

subcortical structures, spinal pathways (habituation & sensitization), amygdala (fear cond), & cerebellum (reflex)

Front 31

What is priming (non-declarative/implicit)?

Back 31

memory effect- exposure to a stimulus influences a response to a later stimulus (list of words, see later if any are familiar)

(demonstrates continual transfer from short to long term memory)

Front 32

Diff btwn anterograde & retrograde amnesia

Back 32

anterograde- inability to form new memories

retrograde- inability to retrieve stored memory

*both due to pathology

Front 33

Describe neural changes involved w/ habituation

Back 33

presynaptic neurons less sensitive
(decreased strength of synaptic connection)
(decreased NT vesicles available for release)

Front 34

Describe neural changes involved w/ sensitization

Back 34

presynaptic neurons more sensitive
(post tetanic potentiation)
(increased Ca in presynaptic terminal, brings closer to threshold for next stimuli)
facilitory interneuron enhances NT release

Front 35

short term sensitization in presynaptic sensory neuron occurs by.......

Back 35

-activation of metabotropic receptor & second messengers (cAMP & PKA, DAG & PKC)
--broadened AP via K+channel inhibition
---increase Ca influx & vesicle release
or
--more vesicles mobilized by MPK (PKA activated) phosphorylation of Synapsin
= activation of motor neuron

Front 36

long term sensitization in presynaptic sensory neurons occurs by.........

Back 36

-MAPK (PKA activated) phosphorylates CREB (transcription factor)
--CREB changes gene epression
---leads to new protein synthesis
----makes facilitation more permanent

Front 37

What are the long term effects in the postsynaptic cell?

Back 37

gene expression changes
changes in physical connections

(necessary for memories to persist long term)

Front 38

Long term potentiation depends on ________ increase in the postsynaptic cell

How does this occur?

Back 38

calcium increase


NMDA ((glutamate) receptor & Ca channel) is activated by Mg+ & causes Ca influx

Front 39

Ca release is only possible when the postsynaptic membrane is 1st depolarized by ______________

Back 39

glutamate binding to AMPARs


(occurs due to increase Ca in synaptic cleft)

Front 40

Increased activity in the postsynaptic cells results in activation of ________________.

What does this do?

Back 40

nitric oxide synthase (generates NO)


NO produces permanent changes in presynaptic terminal to enhance glutamate release w/ APs

Front 41

Pre & postsynaptic changes leads to what?

Back 41

ability to activate synapses normally silent under same conditions (silent synapses)
*sensitization

(mechanism for forming new circuitry in memory)

Front 42

The (early/late) phase of memory formation requires de novo proteins synthesis

For what?

Back 42

formation of new synapses

(via CREB-1 binding to genes & regulation transcription)

Front 43

what is the primary modification to postsynaptic cells?

Back 43

modification of spines on dendrites

Front 44

How can long term depression occur?


Where does it occur?

Back 44

-by long term low freq stimulation
--depresses excitatory potential
--lowers Ca stores
---decreased AMPA receptors (# (via internalization) & sensitivity (via depohsphorylation))

*occurs in cerebellum