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Brain and Behavior > Learning and Memory > Flashcards

Learning and Memory Flashcards

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The Brain flashcards
1
Q

What is learning?

A

Acquisition of information

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2
Q

What is memory?

A

Storage and retrival

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3
Q

How is a memory formed?

A
  1. Acquisition: exposure, saliency, attention, context
  2. Consolidation: short-term into long term memory
  3. Storage: what we do with long term memories
  4. Retrival: bringing out information when we need it
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4
Q

What are the three types of memory?

A
  1. Sensory: unlimited capacity but has very short duration. Can forget it or pay attention to it and it will be transferred
  2. Short-term memory: forget it or reherse it to get it into long-term memory
  3. Long-term memory: forget it
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5
Q

What is short-term memory? How much info can it hold and how long does it last?

A

Working memory

  • capacity: 7 +/- 2 (chunk info to make it easier to remember)
  • lasts an avg of 15-30 seconds
  • depends on rehersal and type of list
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6
Q

What is delayed match to place suppose to test?

A

Working spatial memory. Have to use cues around the room to find the platform to deteremine the location of the platform. How quickly they find and the length of distance is tested. Change location daily

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7
Q

What results did they see in mice that had their hippocampus lesioned in the delayed matching to place task?

A

Mice with lesions did not get much faster over the days

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8
Q

What is long term memory?

A 
•Reference memory
•Long retention interval
–A lifetime
•Large capacity, possibly infinite
•Dependent on short-term: don't have a lot of consolidation
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9
Q

What are the different types of memory?

A 
•Procedural memory (implicit)
–Automatic responses without conscious control (how to)
•Declarative (explicit)
–Memory of information
•Semantic (factual)
•Episodic (personal)
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10
Q

Where are the different types of memory stored in the brain?

A

Cortex: Episodic, Semantic, Priming
Cerebellum: Conditioning
Basal Ganglia, Motor cortex, Cerebellum: Skill learning

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11
Q

What are the components of classical conditioning?

A 
–Unconditioned stimulus (US)
–Unconditioned response (UR)
–Conditioned stimulus (CS)
–Conditioned response (CR)
US produces UR
US paired with CS produces UR
so CS produces CR
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12
Q

What is contextual fear conditioning?

A
  • Context (CS) is paired with an aversive stimulus (US)

* Freezing in response to CS

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13
Q

What effect does giving a betablocker after training have on STM and LTM? How about giving the betablocker before training?

A
  • When the drug is given prior to learning the animal shows no deficit (drug doesn’t disrupt learning process)
  • If you give drug after training you see deficits in STM and LTM (drug effects consolidation process)
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14
Q

What is reconsolidation and what does it do to memory

A
  • Bringing a LTM into active state (reactivation)
  • Once memory is reactivated it has to go through reconsolidation to bring it back to inactive state. New proteins have to be produced
  • Allows you to update memories but they are vulnerable to interference
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15
Q

What is forgetting and what affects it?

A
  • Memory failure
  • Allows us to select the best information
  • Affected by time and disruption in acquisition, consolidation, storage, or retrieval of memory
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16
Q

What is proactive interference?

A

Current memory is disrupted by an earlier memory

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17
Q

What is retroactive interference?

A

Past memory is disrupted by subsequent information

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18
Q

What is retrograde amnesia?

A

–Lose memories prior to damage

–Can form new memories

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19
Q

What is anterograde amnesia?

A

–Lost ability to form new long term memories

20
Q

What is the primacy effect

A

words heard first

–Anterograde amnesia

21
Q

What is the recency effect?

A

words heard last

–Delay before recall

22
Q

What areas of the brain are involved in declarative memory formation?

A

Requires the hippocampus, dorsal medial thalamus, mammillary bodies

23
Q

What is Korsakoff syndrome?

A

Usually occurs in alcoholics. They have low thymine levels (from malnutrition) which leads to destruction of the mammillary bodies. End up with anterograde amnesia.
-Confabulation: make up elaborate story about things and they don’t remember what they said so if you ask them later they will make up another story

24
Q

What does evidence show about procedural memory in people with anterograde amnesia?

A
  • People have damage to hippocampus and amygdala
  • other structures are involved in forming procedural memories. Even though these people don’t remember using the loom, their performance indicates that they do
25
Q

What is neuroplasticity?

A

ability of the brain to change itself in response to things you encounter

26
Q

What are the forms of neuroplasticity?

A
  • Cortical reorganization: sensory and motor cortex, moving connections and having one area of the brain take over for another area
  • Synaptic plasticity: modifying how synapses are connected to one another
  • Neurogenesis: birth of new neurons
27
Q

How can synaptic plasticity be changed?

A

Changes in pre or post synaptic cells

  • amount of NT released (pre)
  • increase in receptors (post)
  • increase in size (pre and/or post)
  • mediated by competition or growth of new synapses
28
Q

What is a Hebbian Synapse?

A

Neurons with higher frequences of AP are stronger synapses so their connections get stronger. There is competition between synapses. Weak are lost while strong are strengthened

29
Q

What is long term potentiation?

A

Give a stimulus and you get a little blip in EPSPs in the postsynaptic cell. You then deliver a tetanus stimulus (results in a lot of AP) and you get a lot bigger EPSP. Then you go back to the weak stimulus. You get a much bigger response to the same stimulus (potentiation). Can last for a while. Basis of how we may be formating new memories

30
Q

Describe the mechanism of LTP

A
  1. Glutamate is released from presynaptic cell
  2. Glutamate binds to AMPA and NMDA receptors on the postsynaptic cell
  3. AMPA is activated and it depolarizes the cell (which causes NMDA receptor to become activated)
  4. Ca flows into postsynaptic cell and activates CaMKII
  5. CaMKII cause latent AMPA receptors to get inserted into the membrane (increasing receptor density) and also sends retrograde signals back to presynaptic cell and cause an increase in NT
31
Q

What is neurogenesis?

A

•Generation of new neurons from stem cell (progenitor cell) population
–Embryonic development
–Adulthood

32
Q

What are some potential application for neurogenesis?

A

•Repair damaged neural tissue
– Brain injury, spinal cord injuries, Parkinson’s disease, Alzheimer’s disease etc…
•Cellular model of learning/memory

33
Q

What do we know about neurogenesis in adults?

A

•Minimal recovery following injury to the central nervous system
•Complexity of the brain
–Difficult for new neurons to integrate
•Structure remains constant

34
Q

Describe neural stem cells

A

–Undifferentiated
–Self renew
–Multipotency

35
Q

Describe progenitor cells

A 
–Undifferentiated
–Limited self-renewal and proliferative capacity
–Generate differentiated cells
•Neuron
•Astrocyte
•Oligodendrocyte (Myelin sheath)
36
Q

How are neural stem cells and progenitor cells different?

A

Progenitor cells have a limited self-renewal and proliferative capacity

37
Q

What regions of the brain engage in neurogenesis?

A

•Olfactory bulb
–Subventricular zone (SVZ) of the lateral ventricle
•Hippocampus: learning and memory

38
Q

What part of the hippocampus is capable of neurogenesis?

A

Granular cell layer of the dentate gyrus

  • stem cells reside in subgranular cell layer
  • stay in the granular layer
39
Q

What happens to the majority of new neurons produced in the hippocampus?

A

They die (90-95%)

40
Q

Describe integration of new neurons into the hippocampus.

A

•New neurons that survive integrate into the granular cell layer
•Granular neurons
–Glutamatergic neurons
–Input from entorhinal cortex (sensory info.)
–Project axons to CA3
–Hyper-excitability

41
Q

How do we detect the presence of new cells?

A

•5-bromo-2-deoxyuridine (BrdU)
–A thymidine substitute: insert into DNA where thymine would usually go
•Immunohistochemistry
–Antibodies label molecules
•Apply additional markers to determine the type of cell the new cell differentiated into
–Neuron (NeuN; neuronal nuclear antigen)

42
Q

How do we regulate hippocampal neurogenesis?

A 
•Process:
–Proliferation
•Number of cells born
–Cell survival
•Number of cells that survive/integrate
–Cell differentiation
•Proportion of new cells become neurons, astrocytes, or oligodendrocytes
43
Q

What factors increase neurogenesis?

A 
–Healthy diet/dietary restriction
–Exercise
–Environmental enrichment
–Learning
–Antidepressants
44
Q

What factors decrease neurogenesis?

A 
–Poor diet/malnutrition
–Stress
–Aging
–Inflammation
–Sleep deprivation
45
Q

How does exercise enhance hippocampal neurogenesis?

A

–Increases in new cell survival

–Increases the proportion of new cells that differentiate into neurons

46
Q

What mechanisms are involved in exercise-induced increase in neurogenesis?

A

•Increased production of neurotrophic factors
–Brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF), and insulin-like growth factor (IGF)
•Growth of new blood vessels (angiogenesis)
•Increases neural activity in dentate gyrus

47
Q

What is epigenetics?

A
  • Genotype – genetic information
  • Phenotype – characteristics expressed
  • Modifies the phenotype without altering the genotype of a cell.

Brain and Behavior (4 decks)

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