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KINE 3670 > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

What are the 3 germ layers of embryo?

A

Ectoderm (outer), mesoderm, endoderm (inner)

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2
Q

What does ectoderm turn into?

A

Skin, neural tissue

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3
Q

What does mesoderm turn into?

A

Muscles, bones

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4
Q

What does endoderm turn into?

A

Internal organs

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5
Q

What does the neural tube eventually turn into?

A

Brain and spinal cord

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6
Q

Where does neural plate form?

A

Dorsal surface of ectoderm

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7
Q

What is spina bifida?

A

Incomplete close of neural tube

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8
Q

What can help prevent spina bifida?

A

Folic acid prenataly

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9
Q

What causes synaptic delay?

A

Waiting for voltage channels to open, waiting for fusion and release of NT, waiting for diffusion and binding

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10
Q

What are two types of receptors of post synaptic membrane?

A

Gpcr (metabotropic) ligand hated (ionotropic)

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11
Q

What do neurotransmitter reiptake transporters do?

A

Remove NT from synaptic cleft so they. Sm be repackaged in vesicles

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12
Q

Are ionotropic or metabotropic faster?

A

Ionotropic ( direct)

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13
Q

How many subunits in ligand gated ion channel?

A

5, 2 alphas, beta, gamma, delta

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14
Q

How many transmembrane (TM) domains does each subunit of a ionotropic receptor have?

A

4

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15
Q

Which transmembrane domain forms the pore in ionotropic receptors?

A

M2

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16
Q

What creates the ligand binding site in ionotropic receptors?

A

Extracellular N terminal domain

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17
Q

How many tm domains do gpcr havr?

A

7 (no ion channels)

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18
Q

What does extracellular site in metabotropic do? N or C terminus

A

Binds NT, N terminus

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19
Q

What does intracellular site in metabotropic do? N or C terminus

A

Binds G protein, C terminus

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20
Q

What are metabotropic receptors involved with?

A

Synaptic plasticity, learning and memory

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21
Q

What class of enzymes add phosphate groups?

A

Kinases

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22
Q

What class of enzymes remove phosphate groups?

A

Phosphatases

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23
Q

How is de-phosphorylation regulated?

A

second messengers

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24
Q

What are the steps of metabotropic receptors?

A

NT binds, g protein is activated, a subunit of g protein binds to effector protein, produces 2nd messenger (cAMP), activatrd PKA

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25
Q

What does PKA do?

A

phosphorylates ion channels, transcription factors, which activates calcium cchannels

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26
Q

What effect doess PKA phosphorylating ion channels have in cell?

A

Na+ ions flow into cell, changes membrane potential

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27
Q

What effect doess PKA phosphorylating transcription factors (ex. CREB) have in cell?

A

activates gene expression and cellular responses

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28
Q

Ca2+ entry into cell activates what specifically?

A

CaMK, which phosphorylates more TF’s and causes more gene expression

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29
Q

What are some examples of CREB sensitive genes?

A

neurotrophin BDNF, tyrosine hydroxylase, immediate early genes

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30
Q

What does neurotrophin BDNF do?

A

promotes neuronal survival

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31
Q

What does tyrosine hydroxylase do?

A

catecholamine synthesis

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32
Q

What do immediate early genes do?

A

IEGs are implicated in learning and memory, and long term potentiation

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33
Q

When are thin and stubby spines more prevalent in brain?

A

immature brain

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34
Q

What is the most prevalent tye of dendritic spine?

A

mushroom

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35
Q

What are post synaptic densities composed of?

A

L-glutamate NT receptors

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36
Q

What does calcium effect in neurons?

A

membrane potential, release of NT, neurite growth and growth cone migration, regulates gene activity

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37
Q

What do EPSP result in?

A

depolarization via entry of Na+ ions

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38
Q

What do IPSP result in?

A

hyperpolarization via entry of Cl- ions

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39
Q

What are type 1 synapses?

A

excitatory, glutamergic, on dendrites, round vesicles

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40
Q

What are type 2 synapses?

A

inhibitory, gabaergic, on cell bodies, flat vesicles

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41
Q

What is spatial summation?

A

summation of inputs from multiple synapses

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42
Q

What is temporal summation?

A

summation of inputs from single synapse over timee

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43
Q

Where are gap junction found?

A

early embryonic stages, in brainstem, between astrocytes, some interneurons in cerebral cortex, thalamus, cerebellum, hypothalamus

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44
Q

What do gap junctions allow through them?

A

ions, molecular with large molecular weights, ATP, second messengers

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45
Q

What type of synaptic communciation is bidirectional?

A

electrical

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46
Q

Is electrical or chemcial synapses faster?

A

electrical

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47
Q

What are some problems with electrical synapses?

A

difficult to modulate the gating of channels, can’t change signs (always flows downhill)

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48
Q

What are active zones?

A

sites of NT release

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49
Q

What are the steps of chemical synaptic transmission?

A

NT are made and stored, action potential arrives, depolarization opens voltage gated channels, influx of Ca2+, NT is released via exocytosis, NT binds to receptor, causes EPSP or IPSP, removal of vesicle via endocytosis

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50
Q

What are the three criteria for something to be a neurotransmitter?

A

must be made and present in presynaptic terminal, must be released in response to depolarization and be Ca2+ dependent, must be a specific receptor, mut be mehcnaism to remove, effects are reproduced by known agonists

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51
Q

What type of synaptic transmission can change signs?

A

chemical

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52
Q

What is quanta?

A

amount of NT released frm a vesicle

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53
Q

Is the docking of synaptic vesicels reversible?

A

no

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54
Q

What are the eight steps of NT release and recycling?

A
  1. NT are actively transported into vesicles
  2. vesicles go in front of active zone
  3. they dock
  4. primed
  5. Ca2+ causes fusion/pore opening
  6. vesicles are taken up by clathrin coated pits
  7. vesicels are reacidified and refilled with NT directly
  8. also could be filled after passing through endosomal intermediate
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55
Q

What are the 3 SNARE proteins?

A

synaptobrevin, syntaxin, SNAP 25 (docking)

synaptotagmin (Ca2+ sensor)

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56
Q

What is the function of synaptotagmin?

A

Calcium snesor, regulates fast exocytosis at synapse

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57
Q

What do the 2 cytoplasmic domains of synaptotagmin do?

A

bind 5 Ca2+ ions

the affinity for calcium ions increases when vesicles bind to membranes

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58
Q

What does mutations in synaptotagmin cause?

A

loss of fast exocytosis

lethal

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59
Q

The priming of synaptic vesicles is dependent on what?

A

ATP

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60
Q

Why are NT stored in vesicles?

A

protection from degradation, sotrage system, concentration, regulation

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61
Q

There is a big difference in the concentration in cell, where is the concentration greater? (Calcium)

A

greater outside cell

less inside

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62
Q

When researchers injected a calcium buffer what did they find?

A

presynaptic current and postsynaptic response were gone

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63
Q

What are the four main roles of calcium?

A

contributes to electrical prperties of neurons by changing membrane potential, release of NT, neurite outgrowht and growht cone migration, regulates geene activity

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64
Q

Is the pre/post synaptic terminals closer in electrical or chemical?

A

closer in electrical

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65
Q

What are excitable cellss?

A

can be stimualted to make an electrical current

muscle/nerves

66
Q

Do only excitable cells have a resting potential?

A

no all cells do

67
Q

What is the resting potnetial?

A

-70mV

68
Q

What causes the resting potential?

A

Na+/K+ pump, leaky potassium channels

69
Q

How much potassium and sodium is transported by the pump?

A

2 K+ in the cell and 3 Na+ out

net loss of positive charge

70
Q

What is the ratio of the concentration of sodium ions?

A

outisde is 10x greater than inside

71
Q

What is the ratio of the concentration of potassium ions?

A

inside is 20x greater than outisde

72
Q

Electrical potentials are genarated across membrane of neurons because?

A

differences in concentrations of specific ions, membranes are selectively permeable to some ions

73
Q

What allows ions to move agaisnt their concentration gradient?

A

ion transportors/pumps

74
Q

What type of transportation does not need ATP?

A

ion channels

75
Q

Are there more non gated Na or K channels?

A

more ungated K+ channels

(leaky channels)

76
Q

At resting potential the membrane is more permeable to?

A

K+ ions

77
Q

What can stimulate gated channels?

A

voltage, ligands binding, mechanical force like stretching

78
Q

What does the Nernst equation predict?

A

equilibtium potential for a single ion

79
Q

What is the Nernst equation? What do the variables stand for?

A

58/z log[x]o/[X]i

z is the charge of ion
[X] is concentration of ion inside and outside

80
Q

Each ions nernst calculation contributes to the memrbane potential, how is the size of the contribution weighted?

A

by the permeability of the ion

81
Q

What does the goldman equation consider?

A

takes into acocunt the concentration gradient of the permeant ions and the relative permeability of the membrane ions

82
Q

What is the goldman equation?

A

= RT/F ln P[X]o/P[X]i

if ion is negative flip the division so inside over outside instead

add the different divisions together

83
Q

What are some types of voltage gated channels?

A

Na+, K+, Ca2+

84
Q

What are some types of ligand gated channels?

A

nAChR, GABAaR, GluR, GlyR

85
Q

Where are voltage gated channels found?

A

muslces and neuronal cells

86
Q

How many subunits in Na+/Ca2+ channels?

A

4 homologous ones

87
Q

How many transmembrane domains in each subunit of Na+/Ca2+ channels?

Which one is voltage sensor, which form pore?

A

6 (S1-S6)

S4, S5 and S6

88
Q

Describe the structure of potassium voltage gated channel?

A

5 subunits, each repeated 4 times to form pore

89
Q

Where is the inactivation gate located on voltage gateed channels?

A

N terminus

90
Q

What is the voltage sensor made up of?

A

positively charge amino acids (arginine, lysine)

91
Q

Why does voltage sensor lay flat closing pore at rest?

A

positvely charged amino acids are attracted to residues of S2 and S3 and negatviely charged inner membrane

92
Q

Why does voltage sensor rotate vertical during AP?

A

as membrane becomes positive it repels the amino acids in sensor

93
Q

What is cell attacehd recording?

A

pipette makes contact with intact cell, measures current of single channel

94
Q

What is inside out recording?

A

pipette attached to cel and then withdrawn the cytoplasmic side of channel is exposed, for single channel recording

95
Q

What is microscopic current?

A

measuring current through single channel

96
Q

What can the patch clamp determine?

A

the molecular composition of ion channels, when signle ion opens/closes, changes in configuration upon opening/closing, channel specificty

97
Q

Why is action potential initiated at axon hillock?

A

lower threshold, smaller diameter, higher desnity of Na+ channels, the Na+ channels here are slow inactivating

98
Q

What is subthreshold stimuli?

A

stimuli that fail to elicit an action potential

99
Q

What is all or none mean in reference to acction potential?

A

you either have an AP or not, no in between

100
Q

What causes the refractory period?

A

inactivation of sodium channels

101
Q

Do sodium or potassium channels open quicker?

A

sodium channels open faster

K+ is slow to open/close (helps restore resting potential)

102
Q

What drives depolarization?

A

increase in permeability of Na+

103
Q

What drives repolarization?

A

fall in permeability of na+ and K+

104
Q

Why does the hyperpolarization phase happen?

A

K+ channels take longer to clsoe, so more K+ is leaving the cell than normal, so it gets more neagtive

105
Q

What is it called when an action potential can be triggered but needs stronger stimulus?

A

relatvie refractory period

106
Q

How many genes for Na+ voltage gated channels?

A

at least 9

Nav 1.1-1.9

107
Q

Where are Nav 1.2 channels located?

A

non myelinated axons

after myelination there is a loss of these channels

108
Q

Where are Nav 1.6 channels located?

A

clustered at nodes of ranvier, only myelinated axons, not detecable under myelin

109
Q

Do Na 1.2 or 1.6 channels have larger current?

A

1.6 does

110
Q

What does the rate of conductance depend on?

A

passive and active flow of current, size (larger cells conduct faster), myelin, size of Na influx

111
Q

Why do larger cells conduct faster?

A

becuase they have better passive flow

112
Q

How fast do action potentials confuct down myelinated and unmeylinated?

A

0.5-10 m/s (umnyelin)

150 m/s (myelin)

113
Q

Where is active cuurrent and passive current in myelinated axon?

A

active is nodes of ranvier

passive is under myelin

114
Q

What is multiple sclerosis?

A

autoimmune, patches of demyelination in CNS

115
Q

What are some symptoms of multiple sclersis?

A

weakness and clumsiness, stiffness/gait disturbances, visual defects, mental defects (lack of judgement, emotional liability, sudden weeping/laughter)

116
Q

What is the most common neurodegenerative disease of young adults?

A

multiple sclerosis

117
Q

What gender is multiple sclerosis most common in?

A

women

also mainly affects caucasians

118
Q

What is an example of a gene that causes MS?

A

MHC (on chromosome 6)

119
Q

What are some environmental agents that cause MS?

A

measles, munmps, herpes, minerals, chemical agnets

120
Q

What is MHC?

A

major histocompatibility complex

encode cell surface antigen presenting proteins

121
Q

What is an epitope?

A

regions of proteins that can trigger a cellular immune response mediated by T or B cells

122
Q

Which class of MHC is involved with MS?

A

Class II

123
Q

Where is MHC Class II found?

A

on specialized antigen-presenting cellls (APCs) macrophages

124
Q

Whaat do MHC Class II interact with?

A

CD4+ t cells (aka. helper t cells)

they divide rapidly and secrete cytokines that help immune response

125
Q

Can white blood cells cross the BBB?

A

not in healthy people

they can in MS

126
Q

What happens during the inflammartory stage of MS?

A

initial infection happens and is processed by macrophages, they display the antigen with MHC molecules, this is recgonized by t cells which activates th1 cells in blood, travel to CNS and encounter local APCs which display a self antigen, reactivates th1 cells which secrete cytokines

127
Q

How are th1 cells able to cross BBB in MS?

A

travel from blood to BBB, bind to adhesion molecules on surface of BBB endothelium, secrete proteases that breakdown the BBB

128
Q

What do cytokines do?

A

stimulate microglia/astrocytes, recruit macrophages and B cells, make more cytokines and antibodies

129
Q

Why does partial recovery happen in MS?

A

there is an increase in the number of channels along the unmyelianted part

more Na1.2

130
Q

Why is there increased intra axonal Ca2+ in MS?

A

because there are more Na/Ca exchangerss

131
Q

How are myelin/axons damaged in MS?

A

cytokines, B cells, direct complement activation, increased Ca2+, increase of free radicals, nitric oxide formation

132
Q

Does remyelination happen?

A

yes but limited, usually myelin is thinner and shorter internodes

133
Q

What allows remyelination to happen?

A

oligodendrocyte precursor cells, neural precursor cells, stem cells

134
Q

What inhibits remyelination in MS?

A

loss of oligodendrocytes and OPCs, inhibitory signals by inflammation, obstruction of oligodendrocytes by astrocytic scars, inhibitory signals between axonal proteins

135
Q

Demyelination-induced axon loss is?

A

irreversible

136
Q

What causes the progressive disability in MS?

A

axon damage and degeneration along with neuron loss (brain atrophy)

137
Q

What are the four types of MS?

A

benign, relapsing-remitting, secondary-progressive, primary progressive

138
Q

What does benign MS look like?

A

stable, gets worse goes back to stable and repeats

139
Q

What does relapsing-remitting MS look like?

A

stable and then gets worse , goes back to stable but slightly worse basline, repeats

140
Q

What does secondary progressive MS look like?

A

like relapsing remitting but then it becomes steaadly progressive

141
Q

What does primary progressive MS look like?

A

starts off and continuously gets worse (10-20%)

142
Q

What are attacks called in MS? What are they preceeded by?

A

relapses

can be unpredicatble or after trigers like cold or stress

143
Q

What is thee most common type of MS?

A

relapsing-remitting 85-90%

144
Q

What type of MS causes the most disability?

A

secondary progressive

145
Q

What type of MS mainly presents in people who get it later in life?

A

primary progressive

146
Q

What in the oligodendrocyte membrane are recognized as foregin by T cells?

A

MBP, MOG, MAG

147
Q

How can MS be diagnosed?

A

MRI, testing CSF, visual evoked potentials and somatosensory evoked potentials

148
Q

What do MRI look like in people with MS?

A

bright lesions show demyelination, widened lateral ventricles and cortical sulci

149
Q

How does testing CSF show MS?

A

testd for oligoclonal bands which are immunoglobulins (evidence for chronic inflammation)

150
Q

How do VEPs and SEPs show MS?

A

electrical potnetial is recorded after stimulus, people w/MS respond less actively

151
Q

Where are plaques in MS found most likely?

A

optic nerves, brainstem, cerbellum, spinal cord

152
Q

What forms plaques in MS?

A

macrophages containing undigest myelin, axonal debris, microglia

153
Q

What is the most common symptoms of initail attack in MS?

A

change in sensation to face/arms/legs

154
Q

What are some congitive impairments in MS?

A

difficulty performing multiple tasks at once, toruble following detailed instructions, loss of short term memory, emotional instability, fatigue

155
Q

15 years after diangosis how many people need assistnace?

A

50-60%

156
Q

What are some challenges with potential treatments for MS?

A

CNS axons dont have regenartive capabilties, formation of glial scar, presence of myelin associated inhibitory molecules

157
Q

What is a difficulty with the treatment option of steem cells with MS?

A

need to implant stem cells in are with damage

158
Q

What is beta interferon?

A

treatment for relasping-remitting MS, given by subcutaneous injections, glycoproteins with antivirl action, reduces # and severity of relapses

159
Q

What does the synthetic form of myelin basic protein do?

A

inhibits the binding of self MBP to the T cells

160
Q

What are some possible therpies for MS?

A

immunosuppresant, glucocorticoids, antioxidant therapy, antidepressants, muscle relaxants, tranquilizers

KINE 3670 (2 decks)

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