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Neuroscience 402 > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

What establishes neural fate and function?

A

cell intrinsic mechanisms such as transcription factors and epigenetics

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2
Q

How do excitatory and inhibitory neurons form?

A

stem cell generates NE which forms NPCs; NPCs differentiate into neurons with neurotransmitter identity

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3
Q

Where does the first decision to form a neuron occur?

A

At the ectoderm when chordin and noggin diffuse into and induce neural fate

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4
Q

What is the antagonist of neural fate in the ectoderm?

A

BMP

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5
Q

Is the neural lineage the default fate of the ectoderm?

A

yes because dissociated animal cap with no BMP forms neurons

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6
Q

What is driving the default neuroectoderm fate?

A

transcription factors

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7
Q

What are the core transcription factors defining pluripotency?

A

SOX2, OCT4, and NANOG (SOX2 and OCT4 turn on NANOG)

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8
Q

What regulates self renewal in pluripotent cells?

A

SOX2 and OCT4

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9
Q

What transcription factors define neural pluripotent cells?

A

SOX2 and PAX6

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10
Q

What allows SOX2 to bind pluripotent genes?

A

Turn off BMP and turn of OCT4 allows SOX2 to bind other genes

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11
Q

What gives the neural lineage genes in the stem cells capable of being rapidly regulated?

A

SOX2 if it is ready to go

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12
Q

What structure marks key developmental genes in embryonic stem cells?

A

developmental genes are poised so a bivalent chromatin structure marks them

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13
Q

What are the two mechanisms for generating neural lineage?

A

abundantly expressed TF ready to initiate the lineage and permissive chromatin underlying neural genes ready to be expressed

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14
Q

What comes first to determine excitatory or inhibitory neurons?

A

the neuron followed by transcription factors

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15
Q

Which transcription factors establish glutamatergic neurons?

A

NeuroD1/4, ASCL1, Neurog2

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16
Q

Which transcription factors establish GABAergic neurons?

A

ASCL1 and DLX2

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17
Q

What are the steps for neurotransmitter identity development?

A
  1. cell fate determination
  2. migration
  3. axon guidance target recognition
  4. synapse formation (differentiation, maturation, modification)
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18
Q

What is the difference between symmetric and asymmetric division in neuron generation?

A

symmetric: npc forms 2 npcs
asymmetric: npc forms 1 npc and 1 neuron

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19
Q

Why does asymmetric division occur?

A

decreased notch in presumptive pro-neural cells initiates genes in the proneural network

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20
Q

What establishes the initial identity of neurotransmitters?

A

TFs established by morphogens

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21
Q

How are immediate early genes activated during neural activity?

A

they are activated by Ca2+

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22
Q

What are the 2 most common forms of neurodegenerative disease?

A

AD and PD

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23
Q

How is AD identified?

A

extensive atrophy and two types of abnormal deposits (amyloid plaques and tau tangles)

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24
Q

How is AD diagnosed?

A

Clinical symptoms, brain pathology, PET and PIB-PET imaging, biomarkers

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25
Q

3 major pathological hallmarks of AD

A

neuronal loss (shrinkage of CTX and HC and enlarged ventricles)
neurofibrillary tangles
amyloid plaques

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26
Q

Abeta hypothesis

A

increased Abeta production via APP and presenilin 1/2 and no Abeta clearance with presence of TREM2, CD33 and ApoE

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27
Q

How is the Abeta hypothesis supported?

A

Human genetic studies (APP mutations)
dynamic progressive changes of AD
mouse genetic studies (decreased glutamatergic neurotransmission and LTP)
cellular studies

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28
Q

How is the tau hypothesis supported?

A

dynamic progressive changes in AD
mouse genetic studies
tau spreading

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29
Q

GWAS studies identified which cell type in AD?

A

Microglia/neuroimmune

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30
Q

How is PD identifed?

A

resting tremors
abnormal posture
gait difficulties
reduced muscle strength
DA neuron loss
alpha-synuclein and lewy bodies

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31
Q

How is the dopamine hypothesis supported?

A

L-Dopa
animal models using MPTP

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32
Q

The targets of cocaine and amphetamine at DAergic synapse

A

amphetamine inhibits NE reuptake
cocaine inhibits DAT

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33
Q

Can PD and AD be a systemic disorder?

A

yes they very well may be

34
Q

How did the cerebellum evolve?

A

early in vertebrate evolution and is largely preserved

35
Q

What are the two parts of the cerebellum?

A

cortex (cerebellar cortex)
subcortical nuclei (deep cerebellar nuclei)

36
Q

How many layers does the cerebellar cortex have?

A

3 layers

37
Q

What does the cerebellum do?

A

improving motor control by smoothness, coordination, speed
execution of non motor functions
cognitive functions
associative learning

38
Q

What are examples of cerebellar learning?

A

Adaptation of the vestibulo-ocular reflex (VOR)
learned motor performance tasks
eyeblink conditioning

39
Q

What are the 3 lobes of the cerebellum?

A

anterior lobe
posterior lobe
flocculonodular lobe

40
Q

What are the 3 subdivisions in the cerebellar cortex?

A

spinocerebellum
cerebrocerebellum
vestibulocerebellum

41
Q

What is under the cerebellar cortex?

A

deep cerebellar nuclei

42
Q

What are the IP and OP of the cerebellar nuclei?

A

IP from CTX
OP to implement control

43
Q

How is the cerebellar cortex arranged?

A

3 layers organized into repeated sagittal zones- 2 IP and 1 OP

44
Q

What are the 2 IP in the basic circuit?

A

Mossy fibers that IP to CTX
Climbing fibers that IP to CTX

45
Q

How does classical conditioning work?

A

must be a change in the system to account for the altered response to the conditioned stimulus after repeated pairing with the US

46
Q

Why study the hippocampus?

A

essential for certain forms of memories

47
Q

What types of methods were designed to study the HC?

A

microelectrodes, tetrodes, extracellular field synaptic potential and population spikes, intracellular recordings, brain slice preparations, computational modeling

48
Q

Hippocampal anatomy

A

hippocampus proper: CA1-3
hippocampal formation: CA, DG and entorhinal cortex (EC), subiculum, pre- and parasubiculum
hilus: reciprocally connected to DG

49
Q

The two types of circuits in the HC

A

Trisynaptic pathway
direct pathway

50
Q

Principal neurons in the HC

A

Dentate gyrus granule cells
CA1 pyramidal neuron
CA3 pyramidal neuron

51
Q

HC functions

A

place cells and spatial memory
episodic memory
emotion and anxiety
regulation of hypothalamic functions
social behavior

52
Q

The 3 different anatomical axis

A

proximal-distal axis (transverse)
deep-superficial axis (radial)
dorsal-ventral axis (long)

53
Q

What are the HC rhythms?

A

Theta, gamma, sharp-wave ripple

54
Q

Engram

A

physical location where a memory is stored

55
Q

Patient H.M.

A

removed entire HC; couldn’t form new memories and only retained long term declarative memories

56
Q

How is the HC involved in long term memory?

A

HS is involved in making long term memories but can’t be where they reside

57
Q

What are the 4 major themes of memory function?

A
  1. there are different types of memory
  2. each type of memory is processed and stored in different brain regions
  3. formation of long term memories occurs in stages
  4. storage of long term memories is distributed
58
Q

Long term declarative memory (explicit)

A

places, events, facts, people

59
Q

Long term nondeclarative memory (implicit)

A

unconscious, practice piano you get better but you don’t know why

60
Q

short term (working memory)

A

distinct, seconds to minute

61
Q

What could H.M. form memory wise?

A

new long term nondeclarative memories because implicit memories don’t go through the HC

62
Q

consolidation

A

the gradual process of memory storage starting with working memory in the prefrontal cortex and moving through the HC to the temporal lobe neocortex as long term declarative memory

63
Q

Face cells of the temporal CTX

A

neurons that fire in response to a face

64
Q

Delay period neurons

A

are direction selective; role in memory

65
Q

olfactory tract

A

olfactory receptor neurons in the olfactory epithelium project through the cribiform plate-> olfactory bulb which are in glomeruli and where mitral and tufted cells make contact-> olfactory tract projection of mitral and tufted cells-> primary olfactory cortex (medial temporal lobe)

66
Q

How is sweet, umami and bitter taste detected?

A

GPCR type 1 and 2 receptors

67
Q

How is salt and sour taste detected?

A

other receptors and ion channels

68
Q

Taste pathway

A

taste receptor cells on tongue-> cranial nerves VII and IX-> nucleus solitaries-> thalamus-> bilateral taste cortices

69
Q

Smell pathway in drosophila

A

Sensory neurons in antenna and maxillary pulp-> antennal lobe as a first order processing center-> mushroom body and leteral protocerebrum as second order processing centers

70
Q

Signal transduction between mammals and insects during smell

A

Mammal: odorant binds OR and activates G alpha olf; G alpha activates ACIII and generates cAMP; cAMP binds ion channels allowing ion flux
Insect: odorant binds OrX (determines what binds) which causes immediate ion flux through OrX and Or83b

71
Q

Why are xenopus oocytes especially useful in odor research?

A

two electrode voltage clamp electrophysiology

72
Q

What ion flow in for salty taste? sour?

A

salty: sodium
sour: sodium and hydrogen

73
Q

what receptors are used for bitter? sweet? umami?

A

bitter: tr2
sweet: t1r2+t1r3
umami: t1r1+t1r3

74
Q

What are the 3 types of cells that make up taste buds?

A

type 1: no expression of taste receptor
type 2: GPCR expressing
type 3: non GPCR receptor

75
Q

How does drosophila taste?

A

leg or wing

76
Q

Why do we need central processing in addition to peripheral olfactory processing?

A

To create an internal predictive model of the world in order to anticipate the future and choose successful courses of action in response to external environmental changes

77
Q

GABAergic modulation for phase coding

A

presynaptic inhibition: constant from spiking neurons or odor evoked
postsynaptic inhibition: odor evoked fast from spiking interneurons or odor evoked slow from nonspiking interneurons

78
Q

What did strowbridge find about GABAergic inhibition?

A

GABAa receptor sensitive excitatory GABAergic responses in mammalian olfactory mitral cell axons in olfactory bulb

79
Q

How do insects smell vs mammals?

A

insects utilize environmental dynamics and mammals create dynamics by sniffing

80
Q

Why do we need central processing in addition to peripheral olfactory processing?

A

central olfactory system uses past experiences to create internal models of the world that can be used to anticipate future event by identifying and categorizing different odor objects which allows the brain to make predictions about the environment based on past experiences with those odors

81
Q

What component of olfactory processing is crucial for survival and successful adaptation to changing environmental conditions?

A

predictive coding

Neuroscience 402 (2 decks)

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