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PSYC 351D > Learning and memory part 2 > Flashcards

Learning and memory part 2 Flashcards

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1
Q

What is the proposed circuit for explicit memory?

A

Mishkin Model

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2
Q

What are the structures in the Mishkin model?

A
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3
Q

What makes explicit memory conscious?

A

The bidirectional flow

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4
Q

What structures are involved in the proposed circuits for implicit memory in the Mishkin model?

A

Basal ganglia
* Ventral thalamus
* Substantia nigra
* Premotor cortex

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5
Q

What makes implicit memories unconscious?

A

Connection between the basal
ganglia & cortex is unidirectional

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6
Q

What is emotional memory?

A

Memory for the affective properties of stimuli or events

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7
Q

Is emotional memory implicit or explicit?

A

Can be either. Implicit is fear conditioning and explicit is knowing you are scared

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8
Q

What structure is critical for emotional memory? How is it stimulated?

A

Emotionally driven events trigger release of cholinergic and noradrenergic NT that
stimulate amygdala

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9
Q

What is the amygdala connected to for emotional memories?

A

medial temporal structures (explicit),
prefrontal cortex, brainstem, hypothalamus (hormone regulation), PAG (pain), basal ganglia (implicit)

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10
Q

What does learning/memory/ experiences lead to?

A

Structural changes in neurons that end up
modifying existing circuits.
New synapses that modify local
connections – not long distance ones
New neurons being formed especially in
olfactory bulb, hippocampus and frontal
and temporal lobes - taxi study

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11
Q

What happens to synapses before and after experience?

A

Before there is a single synapse on dendritic spine. After there are formation of new synapses from new axon terminals and formation of new synapses from original axon terminals

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12
Q

What happens to synapses for motor neurons involved in sensitization and habituation?

A

Less synapses to for habituation
More synapses for sensitization

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13
Q

Are sensitization and habituation implicit or explicit?

A

implicit

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14
Q

What is habituation?

A

decreased response to a
stimulus that’s repeatedly presented

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15
Q

Describe habituation at the neural level

A

habituation involves
reduced sensitivity of calcium channels (less influx of calcium)
leading to less neurotransmitter release –> less depolarization of presynaptic membrane
* Leads to decrease # and size of sensory
synapses

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16
Q

How does the aplysia (sea slug) show habituation?

A

Decreased withdraw if you keep touching it’s siphon

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17
Q

What is sensitization?

A

an enhanced response to some
stimulus within particular context (usually to a negative/ aversive stimulus)

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18
Q

How does sensitization work at a neural level?

A

Involves action of interneuron which contains
serotonin
* Serotonin released onto presynaptic neuron
causes delay in K+ channel opening = prolonged
depolarized state
* This in turn leads to greater influx of CA+ and
more NT release –> enhanced response
* Leads to increase # and size of sensory synapses

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19
Q

Explain sensitization in sea slug

A

If you electrically touch the tail then you just try to touch the siphon it will be even more mad

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20
Q

Are sensitization and habituation both happening at presynaptic membrane?

A

Yes

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21
Q

What is the structural basis for brain plasticity?

A

Long-term potentiation (LTP

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22
Q

What is LTP? What does it work on?

A

Long lasting increase in synaptic effectiveness
after high frequency stimulation. Works on postsynaptic neuron

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23
Q

Where was LTP first recorded and what did they find?

A

in the hippocampus by Bliss
and Lømø in 1973
Strong burst of electrical stimulation applied to the presynaptic neuron increases amplitude of the EPSP in postsynaptic neuron

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24
Q

What is LTP for? What type of memory?

A

Lay down new explicit memories

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25
For the EPSP to increase in size what must happen?
more neurotransmitter must be released from the presynaptic membrane. * Retrograde messengers (released from post-synaptic) could make presynaptic neuron to release more NT * postsynaptic membrane must become more sensitive (more receptors + dendritic spines) to the same amount of transmitter...or all 3.
26
What is Long-term depression?
decrease in EPSP size after low frequency electrical stimulation
27
How are LTP and LTD related for memory?
If LTP is a mechanism for forming memories, perhaps LTD is a mechanism for clearing out old memories
28
What is the neurochemistry of LTP (excitatory synapses)?
Glutamate acts as a neuromodulator - not the only NT for LTP
29
What receptors does glutamate act on on the post-synaptic membrane?
AMPA receptor NMDA receptor
30
What do the AMPA and NMDA receptors do for LTP?
AMPA become more welcoming. It normally responds to glutamate and allows more Na+ influx which leads to depolarization NMDA receptor (more picky): Normally blocked by magnesium (Mg2+) ions; * Can allow Ca2+ influx if 2 conditions are met
31
What are the two events that must occur in rapid sequence for NMDA receptors to open?
Depolarization of postsynaptic membrane, which displaces Mg2+ from pore * Activation of NMDA receptors by glutamate from the presynaptic neuron
32
What happens at the synapse in response to weak electrical stimualtion?
Because the NMDA receptor pore is blocked by a magnesium ion, release of glutamate by a weak electrical stimulation activates only the AMPA receptor --> not enough for NMDA
33
What happens at the synapse in response to strong electrical stimualtion (depolarizing EPSP)?
A strong electrical stimulation can depolarize the postsynaptic membrane sufficiently that the magnesium ion is removed from the NMDA receptor pore --> now glutamate can bind
34
What happens during weak electrical stimulation after the magnesium is knocked off the NMDA pore?
Now glutamate, released by weak stimulation, can activate the NMDA receptor to allow Ca2+ influx, which through second messenger, increases the function or number of AMPA recptors or both
35
What happens after NMDA receptors open?
Ca2+ enters and alters the postsynaptic neuron (2nd messenger processes). * Increased responsiveness of AMPA receptors to glutamate * Formation of new AMPA receptors * Retrograde messengers that trigger more glutamate release from presynaptic neuron
36
What does raising rats in enriched enclosures do (6)?
increased brain weight. * more dendrites. * more astrocytes. * more blood capillaries. * more synapses per neuron. * increased mitochondrial volume --> Marker of greater metabolic activity
37
Describe the study on brain plasticity and learning a new motor skill in monkeys.
Had monkeys retrieve food from small or large food wells. * Small wells required dexterous movements of one or two fingers, * Large well: the monkeys could put their entire hand
38
What were the results of the study on brain plasticity and learning a new motor skill in monkeys?
After training: more motor cortex region dedicated to digits in small wells condition
39
Describe the study on phantom limb syndrome and brain plasticity.
Indirectly measured the cortical maps in individuals with limb amputations --> cortical re-organization
40
What were the results of the study on phantom limb syndrome and brain plasticity? What does it explain?
After amputation, when the face was stroked with a cotton swab, amputees reported sensations of being touched in the amputated hand May explain phantom limb pain. Brain circuitry for pain is still there but limb is not
41
Explain how epigenetics is associated with brain plasticity?
Learning/ forming new memories is associated with epigenetic mechanisms that in turn mediate synaptic plasticity
42
Explain how gene methylation is related to brain plasticity and epigenetics.
E.g., gene methylation associated with fear learning in conditioning. Blocking gene methylation is associated with failure to learn fear stimulus * Epigenetic tags can be passed on to future generation
43
What are the three hormones that influence brain plasticity?
Estrogen, testosterone, glucocorticoids
44
What happens in the brain due to high and low levels of estrogen?
High levels: More dendritic spines in the hippocampus * Low levels: More dendritic spines in neocortex but fewer in hippocampus (memory decline in menopausal women?)
45
What happens in the brain due to low levels of testosterone?
decrease in spatial ability
46
What happens in the brain due to high glucocorticoids in response to prolonged stress?
kills hippocampal cells
47
How do growth factors effect brain plasticity?
Experience triggers production of neurotrophic factors which in turn help in the development of new neurons, glial and reorganization of neural circuits
48
What does drug use cause that is related to brain plasticity?
behavioral sensitization
49
What does drug use lead to?
progressive increase in behavioral actions – likely due to increases in number of receptors, dendritic growth and synapses in specific brain regions (regions primarily affected by the drug)
50
What drugs cause behavioural sensitization?
psychoactive drugs like amphetamine, cocaine, morphine and nicotine
51
What are three ways to recover from brain injury?
Learn new ways to solve problems * Reorganize the brain to do more with less * Generate new neurons to produce new circuits
52
What is the Three-legged cat solution to brain injury?
When a cat loses a leg, it usually regains mobility, not by growing a new leg but rather by learning how to walk with only three legs
53
What is the three-legged cat solution an example of?
Behavioural compensation
54
What is behavioural compensation? Is it effective?
Most common (and most effective) form of recovery Example: a stroke patient may lose the ability to write with the right hand, but compensate by learning to write with the left hand
55
What is the New-Circuit solution to brain injury?
In response to injury, the brain can form new connections and do more with less
56
What interventions increase recovery significantly in addition to the new-circuit solution?
Behavioral therapy Pharmacological therapy Deep brain stimulation to increase activity in remaining parts of damaged area
57
What is an example of Pharmacological therapy
Nerve Growth Factor improves motor functions in animals with stroke damage to the motor cortex
58
What are two examples of the lost-neuron replacement solution?
Fetal tissue implantation (limited success) Replacement of lost cells
59
When is fetal tissue implantation suitable?
when only a small number of cells are needed
60
How does replacement of lost cells work?
Neurotrophic factors can stimulate brain areas to generate cells that eventually differentiate into neurons and glia --> may be useful for treatment of brain injury

PSYC 351D (9 decks)

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