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Biopsych IWS > Neurobiol of Learning & Memory > Flashcards

Neurobiol of Learning & Memory Flashcards

1
Q

Define learning?

A

Acquisition of new knowledge / information

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2
Q

Define memory?

A

Retention of learned information

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3
Q

What are 2 types of memories? ( D & N)

A

Declarative & NON-declarative

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4
Q

How do we form declarative memory? ( G & E)

A

Generic (reference library: facts, words)
* Explicit (memory with “awareness”; - EG what you wore yesterday- requires CONSCIOUS effort)

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5
Q

how do we form NON- declarative memory? ( IMPLICIT)

A

Implicit (memory WITHOUT AWARENESS: past experience influences current task - “procedural memory”)

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6
Q

What structure is associated with Declarative memory? ( Hippo)

A

Medial temporal lobe (hippocampus)

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7
Q

What structure linked to NON- declarative procedural memory? ( C-A- S)

A

Cerebellum (muscular response),
Striatum (habits, skills)
Amygdala (emotional response)

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8
Q

EG of NON - Declarative Procedural memory? ( MOTOR)

A

learning a motor procedure in response to sensory input)

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9
Q

What is NON-associative learning ?( H & S)

A

change in behavioural response to a “repeated stimulus” (e.g. “Habituation & Sensitisation”)

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10
Q

What is Associative learning?( Classical conditioning & ? )

A

forming associations between events (e.g. classical conditioning & instrumental conditioning)

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11
Q

3 aspects of STM ( short term memory) i?

A

May last seconds or hours
* Easily disrupted (distraction/ head trauma)
* Apparent holding capacity is approx. 7 words*

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12
Q

LTM ?

A

Events/facts held for days/months / years after storage
* Not easily disrupted

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13
Q

How do we learn to associate one thing with another?
(ENGAGEMENT !)

A

The smell of a rose with its flower?
* Need to engage with the target, not just be exposed to it

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14
Q

How do we Learn to remember? Sensory > STM > LTM + ?

A

SEE slide 7 diag.. sensory info > STM > LTM

*For a memory to be stored LT: does not have to be a STM first!
(may be stored due to EMOTIONAL response or conscious effort- EG Spaced-practice (repeating over time) is better than Massed -practice (i.e., cramming)

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15
Q

Neuroplasticity: change in brain function - what assist?

**N-P involves all following Q 15-19

A

Learning & memory contribute to N-P

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16
Q

Define Neurogenesis? ( Hippo)

A

New neurons from precursor cells
Development of new neurons
Occurs in hippocampus

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17
Q

What is Neurodegeneration?

A

Death of neurons and rearrangement of synapses

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18
Q

Changes in Dendritic branching involve?

A

Increases in dendritic branches
* PRUNING of dendritic branches

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19
Q

Long Term Adaptations to Synapses involve? ( P & D)

A
  • Long Term “Potentiation” = enhancement of synapse strength
  • Long Term “Depression” = weakening strength of synapse
    (Strength = ability to produce EPSP to promote action potentials)
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19
Q

Can we grow new neurons? Yes! We have stem cells

A
  • Embryonic (pluripotential stem cells) - taken from fertilised eggs (blastocyst) or:
  • Tissue specific
  • Neural stem cells
  • Development of mature cell depends on exposure to growth factors
20
Q

***Review diagram : slide 10-11 Stem cells to Neurons

A
21
Q

Process of neural stem cells? ( CP > subependyma > new cells re exposure)

A

Neural stem cells manufacture (CP) “progenitor” cells

  • CP cells migrate out of subependyma - form new neural cells : with exposure to conditions (e.g., growth factors such as BDNF( brain derived neurotrophic factor)
  • Migrate to – Cortex/ Striatum/ Olfactory Tubercles of forebrain:

– neurogenesis also occurs: dentate gyrus of hippocampus

22
Q

Psychiatric disorders and Neurogeneration ( depression/ exercise/ environment )

A

Depression: decreased neurogenesis in hippocampus (dentate gyrus)

  • Antidepressants enhance neurogenesis in dentate gyrus
  • Exercise enhances learning via neurogenesis in hippocampus
    (Regular physical exercise: ? protect against cognitive decline/dementia as we age + Environmental enrichment aids learning and memory)
22
Q

Can we alter neurons that we have ???YES!

A

Neuron death and rearrangement of synapses:

  • Normal neurodevelopment depends on death of some neurons
  • Neurons grow to meet ‘target’ neurons
  • If a growing neuron does not get the growth factors (and guidance) it needs from target cells …they die off
  • Neuron death helps to focus the output of remaining neurons - ( smaller number of postsynaptic cells = selective neurotransmission)
22
Q

Neuron death : ***see diag. slide 15-16

A

Competition/ target neurons / connections ( pruning)

23
Q

Does experience change our neurons? YES!!! ( experience/ environment)

A

Change in response to experiences - neurons grow more dendrites!

  • Animals in enriched environments > greater dendritic branching/ improved learning skills.
24
Q

Like synaptic elimination: dendrites can be pruned back?

A

Use it or lose it!

25
Q

Overview experience and cortical reorganisation ?

A

Our cortex changes to accommodate motor activity that we need / use:

***see diagrams. slide 19

26
Q

Overview CBT and Reorganisation?

A

CBT > reorganisation of our “neural circuits”

27
Q

Changes to synapses? ( synaptic plasticity/ potentiation+ ? )

A

Synapses change in response to experiences
* Synaptic Plasticity = LT changes in how our synapses work
* Long Term Potentiation
* Long Term Depression
((Kalat module: Neurochemistry of learning

28
Q

Aplysia: the sea slug… ( N-P)

A

Much of what learned about neuroplasticity: comes from the sea slug
- extensive studies re neuroplasticity : associated with sensitisation /habituation : gill withdrawal reflex

Similar & Few and large neurons - so easy to study!

29
Q

Specificity of synaptic connections? ( fire together; wire togther + association)

A

Like a muscle: use more > stronger!!!
- “Fire togther: wire together “
- +++ Exposure: EPSP larger > act.pot > synapse strengthened !!!!

  • 2 sens. signals : gap of time re act.pot for both within about 50ms > LINKAGE + STRENGTHENING ( ASSOCIATION !!! )
  • see diagrams slides 24-26
30
Q

Overview Neuron Firing (diff. freq/ affects synaptic connections)

A

Neurons fire at different frequencies (Hz)

-When neurons fire they release NT into synapse
-Frequency means the number of synaptic excitations per second
Low frequency = 1-5 Hz / HIGH frequency = 50-100 Hz
#Differences in firing frequencies : alter communication between synapses

31
Q

Overview Firing Frequency & Neuroplasticity ( LTP + LTD)

A

Long Term Potentiation (LTP)
* Brief high frequency electrical stimulation of an excitatory pathway >to long-lasting enhancement in strength of the stimulated synapses

Long Term Depression (LTD)
* Brief LOW frequency electrical stimulation of an excitatory pathway > to a long-lasting WEAKENING of the strength of the stimulated synapses
* LTP and LTD rely on the function of #GLUTAMATE receptors

32
Q

Overview Glutamate Receptors ( Glutamate/ Metabotropic / NMDA)

A

Glutamate
- Ionotropic & metabotropic receptors
- Ionotropic let in calcium (Ca++) or sodium (Na+)
- Ionotropic - NMDA (N-methyl-D-aspartate)
- Ionotropic: AMPA (a-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid)
- Ionotropic: Kainate receptors

  • Metabotropic (mGluR1 - mGluR7) - linked to 2nd MESSENGER systems
  • NMDA receptors are unique - usually “plugged” with Magnesium (Mg++) …Only when the dendrite becomes depolarised does the Magnesium leave the NMDA receptor (if glutamate is bound) so that positive ions can come into the cell
33
Q

REVIEW Diagrams slide 31-46

A
34
Q

Synaptic Co-operativity ( fire tog. etc. Depo and act.pot. and ?)

A

Cells that “fire together wire together”

  • High frequency stimulation is not enough to cause LTP
  • EPSP in one part of the neuron requires an ACT. POT to occur at SAME time in order to produce HUGE DEpolarisations
  • > propogation (ie more positive to the dendrites from the axon hillock of the firing neuron)
  • Synapses that co-operate to produce this action potential are wired together and can induce firing later on - independently!
35
Q

BCM Theory (synaptic strength)

A

Bidirectional regulation of synaptic strength (up or down)

  • LTP
    *LTD
  • Synapses that are active when cell is weakly depolarised (i.e., only small EPSP…not action potential) will become weaker.
36
Q

See slides 49-57 for diagrams!!

A
37
Q

Neural Plasticity (Neuroplasticity) - AMPA/ NMDA /Memory…

A

Bidirectional regulation of the AMPA Receptor

  • affects how strongly or weakly inputs are received
  • affects future signalling/firing of the neuron in question
  • How does this relate to memory?
    Animal models (Morris water maze): show NMDA receptor antagonists cause animals to ‘fail to remember’. (Antagonists directed at Calcium entry to cell or that block PKC/CaMKII have similar effects)
38
Q

Neural Plasticity & Memory ( maintaining memories/ LTP and LTD )

A

What about ‘maintenance’ of memories?
- occur by changes in intracellular messengers
- (upregulation) > physical change in the neuron
- Synthesis of new proteins/ neuronal circuits (dendritic branching)
- Disassembly of existing circuits (dendritic pruning)

LTP - strengthens connections that our brains require to remember
LTD - prunes unwanted connections to correct incorrectly learnt pathways or to ‘unlearn’ a behaviour (extinction). (NB: increase in phosphatases helps us to forget ‘unimportant’ information - you DONT need to remember everything!)

Memories
* begin as ELECTRICAL signals
* temporarily remain by changes in second messenger systems ( become long-term when synaptic proteins/structures are modified)

39
Q

Summary 1 _ just read answer

A
  • Aplysia : studying N-P of habituation/sensitisation - simple nervous systems/ remain similar between individual slugs
  • LTP has 3 properties of specificity (active synapses become stronger)&raquo_space;>
    1. co-operativity (synapses that are active together, wire together)
    2. associativity (weak inputs paired with strong inputs: become strengthened).
    3. Hebb’s theory : only synapses that are active within “50 ms” of an action potential produce LTP.
40
Q

Summary 2- just read answer

A

LTP : produced by upregulation of CaMKinase II & Protein Kinase C - upregulate AMPA “glutamate” receptors

  • LTD; phosphatases, >DEactivate glutamate receptors

-Activation of AMPA receptors: >opening NMDA glutamate receptors…..Treatment with NMDA receptor “antagonists” >reduce rodent memory

-Memories : “electrical signals” > temporarily stored : in “2nd messenger systems” > stored LT by changes in the neurons.

40
Q

Temporary memory (WM : maintains while in action: PFC- delayed response test)

A

WM tempstorage of information so our actions are ongoing (so you don’t forget what you were doing half-way through something!).

ST retention also means that you can use this to ‘manipulate’ information – (e.g., do a simple maths equation ‘in your head’)

-WM: PFC of the frontal lobe - tested using a “delayed response task” -Subject receives a stimulus (light over one lever (out of 10)) …Light goes off, ….delay period (longer the delay, better the working memory) - Subject asked to press lever that light was over

Card game: memory / or in animal models: T-maze

41
Q

Hippocampus and memory 1 ( signs that HM had …)

A

The hippocampus : involved in several types of memory

H.M. had his hippocampus removed (medial temporal lobe,)
- Intellect /language OK!!
- Suffered amnesia (loss of memory)
- Anterograde amnesia (cannot form NEW memories)
- Retrograde amnesia (cannot remember recent memories before surgery)
- Cannot learn new facts (declarative) - bad at explicit memory (aware)
- Can learn new motor skills (procedural) - ok with implicit memory (unaware)

**H.M.’s condition suggested :hippocampus was more important for some memories than others.

42
Q

Hoppocampus and memory 2 - Declarative and Spatial

A

The hippocampus : Two of the main memory types are:

  1. Declarative (explicit) memory - many of ours are episodic (single events)
    “object recognition” tests - require animals to show which object is familiar and which is novel (rodents)
    “Delayed matching-to-sample task” which is familiar (primates) “Delayed nonmatching-to-sample task” which is new (primates)
  2. Spatial memory - memories of things in space
    “radial arm maze” - rodents (rats learn to enter each arm once for food reward)
    “Morris water maze” - finding the platform submersed in milky solution

***Animals with hippocampal damage have trouble with all of these tasks

42
Q

Memory Loss occurs in Alzheimer’s Disease (ACh : 3 A’s Memory loss

A
  • Neurodegeneration - selective death of Acetylcholine (ACh) cells
  • Slowly progressing Dementia
  • Memory loss
  • Change in personality
  • Apraxia - loss of ability to co-ordinate movements
  • Aphasia - loss of ability to articulate ideas and comprehend written/spoken word
  • Agnosia - cannot interpret sensory stimuli
43
Q
  • *
    *
    Alzheimer’s Disease: Acetylcholine/ Nicotinic/ Muscarinic
A

Patients with Alzheimer’s Disease:

Reduced Acetylcholine (ACh) Acetylcholine … prevalent in brain regions involved in memory
* Hippocampus, cortex and movement
* Striatum

  • Acetylcholine binds to two (cholinergic) receptor subtypes Nicotinic
    Muscarinic
    *The muscarinic antagonist atropine can “disrupt memory processing”.
    *Atropine has also been shown to “inhibit the process of neurogenesis”
  • Acetylcholine is involved in “proliferation and differentiation of neural stem cells”!
44
Q

Summary 3

A

Working (temporary) memory involves the prefrontal cortex and is tested using a delayed response task

  • Amnesia is the loss of memory - anterograde amnesia is the loss of new memories (or inability to form new memories) after brain damage, retrograde amnesia is the loss of memories that have formed recently before brain damage
  • The hippocampus is most important for declarative and spatial memory
  • Declarative memory can be tested by object recognition and spatial
    memory can be tested in radial arm maze or Morris water maze
  • Alzheimer’s Disease is slow degeneration of neurons, with dementia and memory loss
  • Patients with Alzheimer’s Disease have reduced Acetylcholine (ACh)
  • Acetylcholine binds to muscarinic and nicotinic receptors
  • Atropine is a muscarinic receptor antagonist that can disrupt memory processing and neurogenesis
  • Neurogenesis is the development of new neurons

Biopsych IWS (11 decks)

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