Brainscape's Knowledge GenomeTM

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


See full index

Neuro Quiz 3 > 37_Learning and Memory_Jullet - Sheet1 > Flashcards

37_Learning and Memory_Jullet - Sheet1 Flashcards

1
Q

What is explicit memory?

A

conscious, intentional recollection of previous experiences/information (facts)

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

What is implicit memory?

A

unconscious, unintentional form of memory that aids in the performance of a specific task (motor learning, skilled behavior)

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

What is the hippocampal formation (4)

A

hippocampus, DG, subiculum, entorhinal cortex

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

What is involved in spatial recognition? Object recognition?

A

SPATIAL: hippocampal formation. OBJECT: peri-rhinal + para-hippocampal cortices

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

What are the 4 phases of explicit memory?

A

1) encoding, 2) storage, 3) consolidation, 4) retrieval

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

Where is short-term memory stored? Where is it encoded/consolidated? Where is it ultimately stored?

A

Short term storage: pre-frontal cortex. Encoding/Consolidation: Hippocampus. Final Destination: various cortices, but NOT hippocampus!

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

What is LTP?

A

long-lasting activity-dependent increase in synaptic efficiacy at an individual synpase.

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

What are some functional changes that accompany LTP? Structural?

A

FUNCTIONAL: presynaptic NT release + post-synaptic receptor # and function. STRUCTURAL: #, size, and stability of post-synaptic spines

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

What is the perforant pathway?

A

connectional route from the entorhinal cortex to all fields of the hippocampal formation

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

What is the direct pathway of the perforant pathway?

A

Entorhinal cortex –> CA1 -> LTP

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

What is the indirect pathway of the perforant pathway?

A

Entorhinal cortex -> DG -> CA3 -> Schaffer collaterals -> CA1 -> LTP

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

What are schaffer collaterals? What is its functional role?

A

Projections from CA3 -> CA1 via glutamate. Involved in LTP and requires coordinate excitatory activity of pre+post synaptic cell

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

What are place cells?

A

cells in the hippocampus involved in spatial learning; encodes a spatial map of the environment

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

During LTP, what happens in the pre-synaptic cell? (2)

A

1) increased levels of activity, 2) release of glutamate into synaptic cleft

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

During LTP, what happens in the post-synaptic cell? (2)

A

Depolarization via 1) AMPA and 2) NMDA receptors.

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

During LTP, what happens with depolarization of AMPA receptors in the post-synaptic cell?

A

AMPA mediates fast excitatory transmission of action potentials. Think “AMPA receptors get AMPED UP for ACTION potentials!”

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

During LTP, what happens with depolarization of NMDA receptors in the post-synaptic cell?

A

NMDA mediates LTP (via Ca influx)

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

What are some properties of AMPA receptors that allow them to conduct fast excitatory transmission?

A

1) selective for Na/K (conductance for Na»K), 2) low Ca permeability, 3) FAST synaptic current

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

What are some properties of NMDA receptors that allow them to mediate LTP?

A

1) NMDA conducts Na/K, and Ca. 2) During LOW activity, NMDA receptors are blocked by Mg and cannot conduct. During HIGH activity, large depolarizations of AMPA receptors cause a (+) shift in the membrane potential, and the Mg is icked out of the NMDA pore.

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

What two characteristics of LTP?

A

1) Synapse specificity. 2) associativity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is synapse specificity?

A

only the synapse receiving the high frequency stimulation and very near neighbors are potentiated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is associativity?

A

neighboring synapses that are weakly stimulated may be potentiated by stimulation of that neighbor, especially if there is either repeated pairing of the two stimuli or if there is a strong emotional content to those stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are 4 requirements of LTP?

A

1) high frequency activity in pre-synaptic inputs, 2) coordinate depolarization, 3) activation of both AMPA + NMDA receptors , 4) influx of Ca into post-synaptic cell (via NMDA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why is Ca2+ important in LTP?

A

activates PKA, PKC, and CAMKII, which promotes changes in cytoskeletal architecture for vesicle mobilization, post synaptic density, and gene expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What happens if NMDA receptors are inhibited or deleted at CA1?

A

impaired spatial learning + no LTP in the Schaffer collateral pathway

26
Q

Early changes in LTP are characterized by….(4)

A

1) rapid insertion of AMPA receptors into spines, 2) phosphorylation of AMPA receptors to stabilize the newly inserted receptors and increase single channel conductance, 3) dynamic remodeling of actin cytoskeleton for vesicle mobilization and spine formation, 4) increase release of glutamate from pre-synaptic cell via retrograde messengers (NO, BDNF) that diffuse from the post-synaptic cell -> pre-synaptic cell

27
Q

Late changes in LTP are characterized by….(2)

A

1) gene expression, 2) epigenetic changes via CREB phosphorylation (interacts with a coregulator that functions as histone acetylase/methylation)

28
Q

What happens if there is no histone acetylation in hippocampal neurons?

A

memory is impaired

29
Q

What happens in contextual fear conditioning and how does this affect memory?

A

enhanced BDNF methylation in the hippocampal neurons -> impaired hippocampus in contextual fear memory

30
Q

What is LTD?

A

implicated in memory formation; arises with low-frequency activity (dribble of Ca influx) in pre-/post-synaptic synapses. This leads to activation of PHOSPHATASES that dephosphorylate AMPA receptors in the Schaffer collaterals (CA3 -> CA1). This results in an internalization of AMPA receptors, thus lowering of synaptic strength.

31
Q

What is the role of LTD?

A

depotentiate LTP; lowers/resets the baseline synaptic strength at a mid-range to avoid a “ceiling effect”, such that when there is a new event, there is the potential of restrengthening the synapse again

32
Q

How does stress affect LTP/LTD?

A

Stress causes impaired LTP and LTD: stress induces glucocorticoids release from the hypothalamus -> glucocorticoids stimulate glutamate release & increase the insertion of AMPA receptors in the postsynaptic spine, resulting in a NET INCREASE in the baseline level of synaptic strength. Where if there is something to be learned, there is no flexibility in the system and new information can’t be formed/consolidated!

33
Q

What causes hungtington’s disease?

A

loss of MSNs in the caudate putamen of basal ganglia due to CAG repeats

34
Q

How do CAG repeats mediate the symptoms observed in Huntington’s disease?

A

CAG repeats result in a GAIN of function of transcriptional control. This results in increased production of proteins that overwhelms the proteasome, resulting in toxic huntington protein fragments. This affects axonal transport, mitochondrial function, and Ca homeostasis.

35
Q

What causes Parkinson’s disease? (2)

A

1) loss of dopaminergic neurons in the substantia nigra, results in the accumulation of Lewy Bodies (protein aggregates containing a-synuclein and ubiquitin) 2) mutations in Parkin + UCHL1 proteins that normally direct proteins to the proteaome. Results in an accumulation of misfolded proteins that have a toxic effect.

36
Q

What are lewy bodies?

A

protein aggregates containing a-synuclein and ubiquitin that are observed in Parkinsons disease

37
Q

What are Parkin + UCHL1?

A

direct proteins to the proteaome. Results in an accumulation of misfolded proteins that have a toxic effect; observed in Parkinson’s disease

38
Q

In Parkinson’s disease, how does L-dopa/carbidopa therapy help?

A

Since the substantia nigra degenerates in Parkinsons, there is no dopamine-induced activation of the caudate putamen. Thus, L-DOPA crosses the BBB and enhances dopamine synthesis and release. Carbidopa blocks dopamine synthesis in the periphery (does not cross the BBB).

39
Q

In Parkinson’s disease, how does partial pallidotomy therapy help?

A

It removes the medial part of the globus pallidus, which minimizes involuntary movements (which occurs after long-term treatments with levodopa)

40
Q

In Parkinson’s disease, where are dopamine-secreting cells usually transplanted?

A

substantia nigra + caudate putamen

41
Q

What is deep brain stimulation (DBS)? In Parkinson’s disease, where does DBS usually occur? What does this result in?

A

DBS: electrode is used to create high-frequency stimulation that produces a functional block. LOCATION: Subthalamic Nucleus. RESULT: Increase impulsivity + risky behavior

42
Q

In Parkinson’s disease, where virus-mediated gene delivery usually occur?

A

near the subthalamic nucleus, where virus-mediated increase in GAD enzymes results in increase production of GABA and subsequent inhibition of the subthalamic nucleus.

43
Q

What is Alzherimers disease caused by?

A

neuronal loss that results in 1) cortical+hippocampal shrinkage 2) enlarged ventricles

44
Q

What are 2 hallmark features of Alzhemiers? How does they affect the physiological aspects of a neuron?

A

1) neurofibrillary tangles of tau protein - alter axonal transport 2) amyloid plaques (APP) - induce inflammation and alter synaptic activity

45
Q

What are tau proteins?

A

bind to microtubules and serve as spacers to help keep them organized into bundles. Hyperphosphorylation of tau results in their dissociation from the microtubules and aggregation into fibrils (paired helical fragments)

46
Q

What are amyloid plaques? How do they form?

A

APP protein are cleaved by secretases, and they help maintain synapse function. Cleavage with b/g secretases results in soluble AB40/42, but these will aggregate at high concentrations. This can be caused by: 1) APP mutations, 2) abnormal AB aggregation, 3) abnormal g secretase, or 4) altered cholesterol levels

47
Q

How does cholesterol level affect production of amyloid plaques?

A

g secretase is found on lipid rafts, and its activity is influenced by changes in cholesterol levels

48
Q

What are some therapies that can be used to treat Alzheimers? (4)

A

1) g secretase inhibitors (block aggregate accumulation, 2) anti-amyloid antibody inhibitors - destroy protein aggregates, 3) AChE inhibitors - increase AChE, which normally declines as the result of loss of basal forebrain neurons, 4) oral DOPA/carbidopa therpay - replace neurotransmitters

49
Q

What is a campenot chamber?

A

compartmented tissue culture setup for evaulating peripheral uptake and retrograde transport

50
Q

What are the functional roles of neurotransmitters?

A

growth, survival, differentiation and electrical excitability. Additional roles in myelination, synapse function, and neurite outgrowth

51
Q

What neurotrophins bind to TrkA?

A

NGF

52
Q

What neurotrophins bind to TrkB?

A

BDNF, NT3, NT4/5

53
Q

What neurotrophins bind to TrkC?

A

NT3

54
Q

What neurotrophins bind to p75?

A

NGF, BDNF, NT3, NT4/5. Death receptor

55
Q

Survival of astrocytes depend on this growth factor:

A

bFGF

56
Q

Survival of Schwann cells depend on these growth factors:

A

CNTF, GDNF

57
Q

Survival of muscle cells depend on these growth factors:

A

BDNF, GDNF, IGF1

58
Q

What is the difference between pro-BDNF and BDNF?

A

PRO-BDNF: higher affinity for p75 receptor; binding can result in cell death. BDNF: has a high affinity for TrkB; binding results in survival

59
Q

What is GDNF? What does it signal through?

A

Glial-derived neurotrophic factor. Binds to membrane receptors (GFRa), which activate RET receptors (with tyrosine kinase activity) to dimerize and autophosphorylate tyrosine residues and stimulate intracellular signaling pathways to induce survival of glial cells

60
Q

Where does neurogenesis occur? (3)

A

1) DG of hippocampus, 2) anterior SVZ, 3) olfactory receptor cells in olfactory epithelium

Neuro Quiz 3 (7 decks)

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