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Block 5: Neuro > Midterm outline > Flashcards

Midterm outline Flashcards

1
Q

midbrain primary morphogen

A

Wnt/BMP

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2
Q

Alar plate

A

sensory region of gray matter = dorsal

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3
Q

Basal plate

A

motor region of gray matter = ventral

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4
Q

astrocytes

A

fibroblasts of the brain

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5
Q

microglia

A

macrophages of the brain

resident immune cells of the brain

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6
Q

genomic methylation

A

remyelination req DNA methylation

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7
Q

Non-genomic methylation

A

myelin sheath req Protein and Lipid methylation

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8
Q

Glycogen synthase

A

catalyzes formation of primary structure

  • Polymerizes alpha1,4
  • Transfers glucosyl from UDP glucose

ACTIVATED WHEN DEPHOSPHORYLATED

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9
Q

Glycogen phosphorylase

A

cleaves alpha1,4 linked glucose until 4 residues form alpha 1,6 linkage

ACTIVATED WHEN PHOSPHORYLATED

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10
Q

Debranching enzyme (“AGL”)

A

has two actions

  1. glucosyl transferase
  2. alpha1,6 glucosidase activity, releasing glucose from branch point
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11
Q

ionotropic

A

direct

rapid postysynaptic responses

receptor is an ion channel

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12
Q

metabotropic

A

indirect

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13
Q

botulism

A

toxin produced by clostridium bacteria

taken up by motor neurons –> causes muscle wekaness/paralysis by impairing NT release at NMJ

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14
Q

tetanus

A

toxin produced by clostridium bacteria

caused by wound infection by clostridium spores

taken up by interneurons that usually offer inhibitory infomration to spinal cord

therefore, release inhibition –> hyperexcitability, esp of extensors; tetanic contractions

loss of synaptic inhibiton on spinal motor neurons

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15
Q

alpa latrotoxin

A

black widow spider

calcium independent NT release –> freq end plate potentials, muscle spasm, cramping, pain

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16
Q

nernst potential for sodium

A

60

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17
Q

nernst potential for calcium

A

125

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18
Q

nernst potential for potassium

A

-90

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19
Q

nernst potential for cl

A

-80

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20
Q

long term potentiaition

A

brief, high freq stimulus train

400 Hz 25 ms

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21
Q

long term depression

A

long (10-15min) low freq (1hz) stimuli

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22
Q

“coincidence detector”

A

NMDA can detect when two are firing at once; those that fire together wire together

Mg needs a certain threshold to dissociate, so know if two axons are firing

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23
Q

Glutamate

A
  • major excitatory transmitter
  • Calcium dep exocytosis
  • synthesized by glia
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24
Q

holoprosencephaly

A

incomplete cleavage of prosencephalon

lateral ventricles fuse

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25
Q

signaling centers

A

generate positional informaion; ANR, ZLI, IsO

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26
Q

hox genes

A

responsible for hindbrain segmentation

convey positional value along AP axis

recall: hindbrain developmental units are the rhombomeres

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27
Q

symmetrical cell division timeline

A

day 0-42

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28
Q

asymmetric cell division timeline

A

starts at day 42

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29
Q

neurogenesis

A

progenitor pool expansion and asymmetric cell division

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30
Q

whats going on in the ventricular zone

A

cells are actively dividing

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31
Q

cause of microcephaly

A

head circumference significantly smaller

due to imbalance between proliferation and differentiation

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32
Q

neuronal migration disorders

A

lissencephaly

agyria

polymicrogyra

neuronal heterotropia

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33
Q

double cortex syndrome

A

band of neurons stuck in white matter

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34
Q

paired pulse short term facilitation

A

residual calcium increases the probability of NT release (presynaptic event)

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35
Q

paired pulse short term depression

A

deplete the NT stores with successive stimuli; presynaptic event

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36
Q

long term potentiation mechanism

A
  • brief, high frequency stimulus = stimulus train = tetanus
  • causes depol that opens NMDA channel, calcium rushes in and then causes more AMPA channels to be inserted on the membrane –> next time, stornger resposne to same stimulus
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37
Q

long term depression mechanism

A
  • long, low freq stimulus
  • depolarization opens NMDA channel and calcium rushes in but due to the length of low freq stimulus, the timing of the calcium activates a dif pathway
  • results in AMPA channels being removed from post-synaptic membrane
    • next time, weaker response
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38
Q

normal synaptic transmission

A

single AP in one or two axons, small EPSP and no LTP; irrelevant stimuli are not remembered

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39
Q

cooperativity

A

strong, coordinated activity (strong input) gives suprathreshold EPSP and LTP; allows for important stimuli to be remembered

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40
Q

associativity

A

stimulation of strong and weak inputs together cause LTP in both pathways; weak stimuli become significant when paired with strong stimulus –> ASSOCIATIVE LEARNING

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41
Q

synapse specificity

A

unstimulated synapse DOES NOT undergo LTP evne if strong stimulation of neighboring synapses

means memories are formed SELECTIVELY at active synapses

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42
Q

enzyme that makes dopamine

A

tyrosine hydroxylase

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43
Q

enzyme that makes acetylcholine

A

choline acetyltransferase

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44
Q

enzymes that makes serotonin

A

tryptophan hydroxylase

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45
Q

PCPA

A

drug that competes with trp and binds irreversibly to TPH (tryptophan hydroxylase)

blocks 5HT synthesis

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46
Q

what kind of gating is the NMDA channel

A

ligand gated

but the magnesium is voltage gated

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47
Q

netrin DCC

A

attraction; for axonal guidance

axons are responsibe only before crossing

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48
Q

Slit roundabout (ROBO)

A

repulsive q

responsibeness is down regulated at the midline, upregulated after crossing

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49
Q

embryonic period

A

week 0-8 of gestation

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50
Q

what do the neural crest cells create?

A

peripheral nervous system!

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51
Q

what are different types of neural tube closure defects?

A

anencephaly =upper portion

spina bifida = lower portion

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52
Q

what are the three primay brain vesicles

A
  1. prosencephalon
  2. mesencephalon
  3. rhombencephalon
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53
Q

what comes from the prosencephalon

A

telencephalon and diencephalon

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54
Q

what comes from telencephalon

A

cerebrum

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55
Q

cortical plate

A

dense, area which is the future cerebral cortex

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56
Q

what causes microcephaly

A

imbalance between proliferation and differentiation causing a depeted progenitor pool and therefore a small brain (can be due to genetic causes or environmental factors)

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57
Q

double cortex syndrome

A

band of neurons stuck in white matter

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58
Q

when does cerebellum develop

A

wk7

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59
Q

when does thalamus develop

A

wk8-9.5

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60
Q

what is the function of arachnoid villi?

A

reabsorb the CSF

if not working–> can cause hydrocephaly

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61
Q

what is the funciton of the choroid plexus?

A

secrete CSF
if not working correctly –> can cause hydrocephaly

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62
Q

sulcans limitans

A

divides alar (dorsal) and basal (ventral) plate cells

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63
Q

spina bifida occulta

A

occurs because the caudal portion of the neural tube does not close properly; therefore there is a bony defect often with a tuft of hair or skin dimple

there is no herniation of either the meninges or the neural tissue

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64
Q

meningocele

A

subtype of spina bifida, which occurs due to the caudal poriton of the neural tube not closing appropriately

the meninges herniates through the bony defect, but the neural tissue remains in place

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65
Q

meningomyelocele

A

subtype of spina bifida, which occurs because the caudal portion of the neural tube does not close properly

both neural tissue and meninges herniate through the bony defect

66
Q

charcot marie tooth

A
  • motor and sensory neuropathy, muscle weakness
  • either defect in protein for myelination or protein for axon transport (mitofusion)
67
Q

mitofusin

A
  • controls mitochondrial transport and fusion
  • mutated in charcot marie tooth
68
Q

NMNAT2

A

axon survival factors; need to get all the way to the distal axon, otherwise, trigger self destruction

69
Q

absolute risk

A

chance of developing the disease

70
Q

relative risk

A

% elevation in risk if risk behavior continues

% reduction in risk if risk behavior stops

RR = incidence in exposed/incidence in unexposed

71
Q

attributable risk

A

excess chance of disease if an exposure continues

72
Q

attributable risk fraction

A

proportion of cases of disease due to an exposure or behavior

73
Q

confidence interval

A

two numbers calculated from sample statistics that determine a range which is likely to include true pop parameter

74
Q

standard error

A

variablility of many sample means

SE = SD/sqrt n

75
Q

a standard error is always ….

A

SMALLER than standard deviaiton

76
Q

what happens as confidence level increases

A

interval widens

77
Q

what happens as the standard error increases

A

interval widens

78
Q

what happens as the sample size increases

A

interval narrows

79
Q

Proportions and variance

A

variance = pq

q = 1-p

stdev = sqrt pq

80
Q

estimation

A

type of statistical inferenec where the statistic estimates a parameter

statistic=sample, parameter=population

81
Q

what does AMPA gate

A

sodium

82
Q

what does NMDA gate

A

calcium entry

83
Q

nicotinic ACh receptor gates

A

Na and K

84
Q

muscarinic ACh receptor gates

A

opens K and closes Ca channels

85
Q

Lambert-Eaton syndrome

A

autoimmune disease; pt makes antibodies to Ca channels

reduced presynaptic release of Ach

tx: drug prevents acetylcholinesterase

86
Q

asymmetric

A

excitatory

have thick post-synaptic density

87
Q

symmetric

A

inhibitory

have equal density on either side

88
Q

natural opiates

A

endorphin neuropeptides

decrease Ca influx

decr NT release

do this by releasing serotonin or NE –> activates opioid interneurons and suppresses spinothalamic tract neurons

may incr K conductnace

opiates decrease the amplitutde of the postsynaptic potential

89
Q

what does the myelencephalon give?

A

medulla oblongata

90
Q

what does the metencephalon give?

A

pons and cerebellum

91
Q

in humans when is cortical neurogenesis completed by?

A

week 16 (day 108)

92
Q

what environmental agents can cause microcephaly?

A

ZIKA virus (or other viral agents) and maternal alcohol consumption (fetal alcohol syndrome )

93
Q

when do gyrations get added to the brain

A

at the end of pregnancy around 9 mo

94
Q

organizing center

A

helps develops boundaries (like isthmic organizer –> between midbrain and hindbrain)

HOX genes end in rhombomere 1 which develops into cerebellum

hindbrain has 8 rhombomeres (variably express hox gene and the expression overlaps)

95
Q

Fgf8

A

secreted by ishthmic organizer the boundary between midbrain and hindbrain

96
Q

retinoids

A

play regulatory role in hox gene expression (induce differential hox gene expression)

vitamin a derivative (vit a deficiency in pregnancy or ingestion of high vit a can cause brain malformation)

considered a morphogen

(pattern of hox gene expression overlaps)

97
Q

B1deficiency

A

pyruvate dehydrogenase

Beri Beri = peripheral neuropathy with parethesis, numbness, pain

Wernike Korsakorff

98
Q

alar plate would be located in which part of midbrain

A

the superior and inferior colliculi

99
Q

basal plate would be located in which part of the midbrain

A

ventrally, motor nuclei; efferents

but dorsal to the SN and CC

100
Q

location of sensory v motor in pons

A

sensory (alar plate) located on side

motor (basal plate) located in the middle

101
Q

what is a key finding with B12 deficiency

A

spinal cord myelin degeneration

102
Q

niacin b3 deficiency

A

this is the ONLY vitamin we can synthesize!!!

serotonin synthesis is impaired due to deficiency in dietary tryptophan

103
Q

folic acid deficiency

A

B9 deficiency

neural tube defect

defective purine and pyrimiding biosynthesis

***impacts the conversion of homocystine to methionine (which is also something that B12 does)

104
Q

Product of SAM methylations

A

is SAH (S-adenosyl homocysteine) which is cleaved to homocysteine

105
Q

Uses of SAM

A

creatine synthesis – major

Norepinephrine –> epinephrine

nucleotides –> methylated nucleotides

phosphatidylethanolamine –> phosphatidylcholine; acetylserotonin –> melatonin

106
Q

where does SAM come from

A

it is a metabolite of methionine

107
Q

causes of B12 deficiency

A

either lack in diet (comes from ANIMAL PRODUCTS because its synthesized by bacteria)

OR

issue with uptake (lack intrinsic factor –> old age, surgery)

108
Q

common neuro symptoms of B12 deficiency

A

diminished vibration sensation with proprioception in legs

weakness

depression

cognitive impairment

109
Q

what induces basal plate

A

SHH

110
Q

risk

A

probability of disease occuring during a defined time period within a defined population that is FREE OF DISEASE

111
Q

risk factor

A

either part of causal chain or exposes indv to causal chain

112
Q

what kind of study is an odds ratio used in

A

case control

113
Q

point estimate

A

a single sample statistic used as an estimate

114
Q

reduced ankle jerk

A

sign of b12 deficiency

115
Q

Lhermittes sign

A

flexing neck results in electrical shock like sensation

sign of B12 deficiency

116
Q

how much of glycogenolysis is accomplished by glycogen phosphorylase?

A

30% then AGL comes in and then afterwards the rest of it can be broken down

117
Q

what are some proteins associated with glycogen

A

phosphorylase –> important because allows activation of glycogen synthase

important b/c without maylin, may get extra proteins hanging out there which can affect the solubility

AMPK is another one associated –> promotes energy generation and inhibits energy consumption; appetitie stimulation

118
Q

AMPK

A

assoc with glycogen

promotes energy generation and inhibits energy consumption; appetitie stimulation

inhibits ACC (acetylcoA–>malonyl CoA)

(ACC=acetylcoa carboxylase)

119
Q

g6P ase

A

astrocytes dont have it so they cant remove the phosphate and cant release glucose; therefore they make lactate

120
Q

what is the product of glycogenolysis in the neuron and astrocytes

A

lactate

121
Q

glial fibrillary acidic protein

A

astrocytes (a type of glial cells) start to release this which is an intermediate

122
Q

myelin basic protein

A

MBP needs to be

123
Q

gap region has

A

progenitor cells

  • neural progenitors
  • glial progenitors
124
Q

dense core vesicle

A

neuropeptide

some NT

125
Q

what two enzymes is B12 a cofactor for

A

methionine synthase

methyl malonyl-co A mutase

126
Q

where is homocysteine converted to methionine

A

cytoplasm

B12 is a cofactor

methycobalamin is the helper

127
Q

where is methylmalonyl co A converted to succinyl Co A

A

mitochondria

adenosylcobalamin is the helper

succinylco a can then enter TCA cycle

128
Q

what kind of methylation is MBP

A

arginine methylated

129
Q

how did they induce demyelination in the mice

A

lysolecithin

130
Q

what systemic result can you see in elevated homocysteine

A

incr inflammation and pro-inflam cytokines

131
Q

what does elevated MMA do to myelination

A

inhibit it

132
Q

what fatty acid results do you see in a methyl malonylco A mutase deficiency

A

aka B12 deficiency, b/c b12 is a cofactor for methyl malonyl co A mutase, which converts methyl malonyl co A to succinyl co A for the TCA cycle

you will get a buildup of branched chain FA

incr propionyl co a will cause formation of odd chain fa

133
Q

where is the majojrity of the glycogen in the brain

A

astrocytes; levels 100x less than in muscle and hepatocytes

134
Q

TGF beta pathway

A

type I and type II receptor (type II is dominant negative)

Transcription factor (Smad)

gene activation

135
Q

necrosis

A

messy, debris, inflammation

provoked

not self initiated

136
Q

neurotorphins

A

essential for development

incldue NGF, BDNF

activate tyrosine receptor kinase receptors

137
Q

cleaved forms of neurotrophins

A

promote survival

(specific for TrkA, TrkB, TrkC)

138
Q

pro forms of neurotrophins

A

activate p75NTR –> TRIGGERS CELL DEATH

139
Q

where do oligodenddrocyte precursor cells come from

A

subventricular zone

140
Q

what signals modulate myelin biogenesis

A

PTEN!!! which modulates Akt/mTOR

141
Q

AKT

A

promotes survival

142
Q

myelin distribution during oligodendrocyte differentiation

A

starts out symmetrical but becomes increasingly asymmetrical as the OLG is contact forming and then myelinating

143
Q

what do ECM factors do to oligodendrocytes

A

laminin and fibronectin bind to receptors on oligodendrocytes

the receptors = integrins and dystroglycan s

this interaction allows signal transduction for regulation of cytoskeleton

144
Q

how do nuclear enzymes disrupt axonal integrity

A

incr inflamm cytokines –> incr ca –> export HDAC from nucleus –> in cytoplasm , HDAC binds the proteins that usually transport mitochondria down the axon

without mitochondria at distal axon, get axonal death

145
Q

BDNF in neurodegenerative diseases

A

alzheimers - incr early , reduce as progression;

parkinsons - delivery of BDNF rescued SN dopa

huntingtons - decr amt

146
Q

REST

A

inhibits BDNF transcription

Wild type huntington keeps REST in cytoplasm –> prevents REST from inhibiting BDNF

mutant huntington –> REST not kept in cytopalsm –> REST enters nucleus –> REST Inhibits BDNF –> bad

mutant huntingtin = reduced funtion and reduced trasnport in both directinos

147
Q

what are the ways huntingtin affects BDNF

A

decr transcription

decr transport

148
Q

strategies to restore BDNF

A

many fancy ones, but really –> diet, exercise, cogntiive stimulation

149
Q

name the layers of SVZ

A

start at lateral ventrical

ependymal layer, gap region, astrocyte ribbon, myelin layer, striatum

source of neurogenesis in adult CNS

150
Q

what makes up the adult subventricular zone

A

migrating neuroblasts

astrocytes

transitory amplyfying progenitor cell

ependymal cells

151
Q

chromatin becomes more/less compact with methyl groups

A

MORE compact

results in reduced expression of inhibitors of myelinaiton

thus, methylation is required for remyelination

152
Q

where are neuronal progenitors

A

ventricular subependymal dentate gyrus

153
Q

glial progenitors

A

subcortical white matter

154
Q

where are progenitor cells found in the subventricular zone

A

gap region

155
Q

what is NO made from

A

arginine

156
Q

does NO need vessicles

A

NOPE!

157
Q

what way do endocannabinooids work

A

they act in retrograde fashion, flosting back to the presynnaptic terminal and suppressing the release of glutamtate (Excitatory)

similar effects true at GABA (inhibitory) synapses

158
Q

what do endocannabinoids derive from?

A

lipid

159
Q

CB2

A

receptor for endocannabinoids that are largely found on cells of immune system

160
Q

CB1

A

endocannabanoid receptor that is found in brain; inhibitory GPCR ; inhibits votage gated calcium channels or stimulates K+ channels

aka has inhib action

161
Q
A

Block 5: Neuro (8 decks)

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