Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Neuroscience Test 2 > Learning > Flashcards

Learning Flashcards

1
Q

Long term memory is divided into these two subgroups

A

declarative and nondeclarative memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

declarative memory

A

things you know that you can tell others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

nondeclarative(procedural memory)

A

things you know that you can show by doing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

relational learning

A

involves the connection or relationship between memories. This needs more info, slide was ambiguous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

contrast semantic and episodic memory

A

semantic info is memory of words, conecepts, facts. knowledge of when or how it was learned is usually forgotten
episodic memory is the memory of events associated with one time, place, and circumstance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is iconic memory

A

the shortest memory. usually something like a picture flashed on a screen (echoic if auditory)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

define short term memory

A

STM usually lasts for 30 seconds or throughout rehearsal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

intermediate term memory

A

outlasts a stm but is not permanent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

long term memory… duh

A

lasts for days to years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Know the trend of memory on the graph plotting time vs. strength of trace

A

general tendency is for memory to decrease from iconic to short term to intermediate. long term gradually increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Recall the info on the slide about sensory memory/ iconic memory

A

hold slarge amount of perceptual input
very brief time
happens automatically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

name the three components of STM/working memory. How is this regulated?

A

phonological loop, visuospatial sketch pad, episodic buffer

regulated/supervised by executive control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

episodic buffer in STM

A

contains more integrated, sensory info

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

STM memory holds how much…

A

7 +- 2, chunking can make it larger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is LTM recalled

A

it must first move into STM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Incoming information is accepted by sensory buffers. It is encoded and sent to short term storage. Where are the three possible destinations for information after STM?

A

Working memory
consolidation to LTM
Trashed… wasted… forgotten 4-eva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

encoding

A

putting new info into memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

retrieval

A

duh. we know about retrieval from amnesia patients case studies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

contrast anterograde vs retrograde

A

anterograde is the inability to form new memories
retrograde is the other one
usually anterograde is accompanied by retrograde

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

look at page 535 for…

A

good review of where memory happens in the brain

21
Q

If you undergo bilateral hippocamp-ectomy you will suffer from

A

anterograde amnesia

22
Q

Tell me about HM

A 
severe anterograde amnesia
normal STM and LTM(events prior to surg)
problems with consolidation of declarative and spatial memories
normal nondeclarative
so... whats the problem
23
Q

korsakoff syndrome

A

caused by alcohol abuse, lack of b1(thiamine), effects diencephalon. further damage to mammillary bodies as wel las dorsomedial thalamus. signs/symptoms i nclude impaired memory, confabulation

24
Q

patinet N.A. what was damaged and what is the problem

A

Na brain was damaged when rod went up his nose and damaged the left dorsal thalamus, bilateral damage to mammillary bodies, and probable damage to the mammillothalamic tract. N.A. shows normal STM but cannot form normal declarative memories.

25
Q

imaging studies confirmed these two regions as important in LTM. When are the activated?

A 
medial temportal (hippocampal)
diencephalic 
They are activated during encoding and retrieving, but the site of long term storage depends on the cortex
26
Q

review slide 19, 20, 21

A

encoding, consolidation, retrieval

27
Q

retrograde amnesia of a few years is caused by specific damage to

A

the hippocampus: specificaly the dentate and subiculum causes loss of a few years of memory

28
Q

retrograde amnesia.. loss of decades worth of memory is a results of damage to the

A

entorhinal cortex

29
Q

London taxis drivers have trained their brain to encompass a large spatial memory. What part of their brain has abnormally large

A

right posterior hippocampus

30
Q

Patient H.M. couldn’t learn his new way environment. why?

A

spatial memories require the right hippocampal formation

31
Q

The ratio of hippocampus to telecephalon volume is different in food storing and non food storing birds. Which has the larger hippocampus?

A

food storing birds on average have larger hippocampi. same concept as london taxi drivers

32
Q

What can or cant HM learn?

A

He has a normal non declarative memory so he can
learn new motor tasks
remember new faces
acquire classically conditioned blink response
but he doesnt remember the episode of learning them (episodic)
he has problems with consolidation of declarati e and spatial memories but his stm and ltm are normal

33
Q

Hebb’s rule

A

a synapse that repeatedly becomes active at about the same time that the post synaptic neuron fires will strengthen the synapse.
neurons that fire together wire together

34
Q

neuroplasticity

A

modifications of gene expression protein expression and protein function

35
Q

describe the neurocircuitry of operant conditioning

A

DA release in nucleus accumbens

over learning involves transfer of locus of control to basal ganglia

36
Q

describe pathways through hippocampus

A

inputs to the hippocampal foration come from nearby entorhinal cortex via axons of the perforant pathway. The axons push through the subiculum. Originally, LTP was demonstrated at sites which consists of synapses from the perforant path to the dentate gyrus. Now, other pathways do it too. The dentate gyrus (mossy fibers) run tot he hippocampus where they synapse in area CA3. In another case, neurons in CA3 send their axons, called schaffer collaterals, to area CA1.

37
Q

damage to CA1

A

anterograde amnesia

38
Q

dentate and subiculum of hippocampus damage

A

causes loss of few years memory

39
Q

damage to entorhinal cortex

A

loss of decades of memory

40
Q

detail LTP in the CA1 region

A

Some synapses have both NMDA and AMPA receptors. If there are only moderate amounts of glutamate in the synapse, only AMPA reacts. this is due to magnesium ions blocking the NMDA channels. Once the cell is depolarized to -35mv, magnesium is removed from the NMDA channels and Ca++ rushes in. The influx of Ca initiates protein kinase to phosphorylate proteins.

41
Q

What does CaM do

A

CaM is a protein kinase that is activated by the influx of Ca when NMDA channels are opened after magnesium is removed at -35mv. CaM does 2 things: it phosphorylates AMPA receptors already present in the membrane of the dendritic spine, thus increasing their conductance to Na and K. It also promotes movement of AMPA receptors to the membrane making more receptors available to stimulate

42
Q

drugs that inhibit CaM kinase interfere with:

A

intermediate term ememory

43
Q

inhibitors of PKC kinase interfere with.

A

long term memory formation

44
Q

describe how protein kinases trigger the synthesis of proteins

A

the kinases phosphorylate and activate CREB (cAMP responsive element binding protein). CREB binds to cAMP responsive elements. CREB activation regulates the expression of many different genes that can alter the growth and differentiation of neurons by changing the rate of transcription of genes.

45
Q

explain retrograde signaling via LTP

A

CREB regulates genes that produce certain proteins. Moreover, 3 hours after induction of LTP, certain proteins increase whle others decrease. Therefore, LTP activates a retrograde signal from the postsynaptic neuron to the presynaptic neuron. It usually instructs the presynaptic neuron to release more transmitter

46
Q

Name the two ways by which LTP increases effectiveness of synapses

A

increases number of postsynaptic receptors

increases the release of transmitter

47
Q

Name some of the proposed molecules responsble for retrograde signaling in LTP

A

NO, arachidonic acid, nerve growth factor

48
Q

Long-Term Depression

A

Low frequency stimulation of a post synaptic cell can decrease the strength of this synapse.
stimulation of the terminal button while the post synaptic cell is
hyperpolarized
reverses previously established synaptic change

49
Q

mGluR5 dependent LTD

A

glutamate binds to mGlur5 receptors causing endocannabinoids to be produced within the post synaptic neuron. endocannabinoids are transported retrogradely to the pre synaptic neuron and prevent the release of glutamate

Neuroscience Test 2 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions