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NeuroBiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

Synapse

A

Physical connection of two neurons that transfer neuronal information from one to the other

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2
Q

Pre synaptic

A

part of synapse sending the info

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3
Q

post synaptic

A

part of synapse recieving the info

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4
Q

Snaptogenesis

A

formation of synapses

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5
Q

Snaptic specificity

A

formation of correct and not incorrect synapseds

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6
Q

PSD

A

post snaptic density
NT receptors and number of protens - helps modulate

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7
Q

Mitochondria in presnaptic

A

make energy (ATPase pumps need, exocotiosis, etc.)

most important
Reupstake (in vessicles)
need high energy sourse to pump NT into vessicels (high and constant demand)

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8
Q

Neurotransmiter transporters

A

reuptake (if not would stay in cleft and bind causing AP)

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9
Q

Snaptic vessicels

A

some with NT in it - fuse with membrane

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10
Q

Chemical synapses

A

clear structural difference between pre and post synaptic
chemical elicit comunication
primaraly in nervous system (slower)
easier to see - easier to study

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11
Q

Electrical synapses

A

No clear structural differences between post and pre synaptic
Ions travel between
Primaraly used for synchronization
more present then chemical synapsed

connect with gap junctions
speed much faster

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12
Q

types of chemical synapses

A

excitatory and inhibitory

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13
Q

Vesicle binding to target plasma membrane

A

protein targets on vesicle and membrane
zippering of proteins (if inhibit this than inhibit NT from releasing)

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14
Q

Why spontanious relese of NT/ vessicles

A

need to be primed for when needed it (so would not want to completely shut of ever, would want to modulate)

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15
Q

spontaious relese

A

vessicle relase NT not in secronized fassion

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16
Q

Patch clamp

A

suck up part of membrane

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17
Q

Need for reflux reaction

A

exitatory neusons and inhibitoyu neurons (so not sence heat once move off)

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18
Q

ionotropic receptor

A

assocated with actual firing event
on or off

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19
Q

metabatropic receptor

A

modulate ion changels
sould be this much on or this much off

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20
Q

Ach (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)

A

Exitatory
Alz

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21
Q

Dopamine (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)

A

Inhibitory
Parkinsins

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22
Q

Serotonin (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)

A

Inhibitory
depression, mood disorders

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23
Q

Norepinephrine (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)

A

Excitatory
mental disorders, depression

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24
Q

GABA (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)

A

Inhibioty
anxiety

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25
Q

Endorphins (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)

A

Inhibitory
body experences pain

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26
Q

Glutamate (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)

A

exitatory
(seesures?)

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27
Q

Steps of Synaptogenesis

A

1 Induce membrane contact
2 Recognition of synaptic partner
3 Induce release of vesicle
4 Depolarize post synaptic cell
5 Recruit PSD scaffold proteins
6 Aggregate PSD receptors
7 Aggregate pre synaptic vesicles

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28
Q

Synaptic specificity is generated by

A

the synaptic guidepost protein SYG2 and its receptor SYG1

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29
Q

Why does the nervous system need glial cells

A

speed, saltatory conduction, nodes of Ranveer

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30
Q

microglia deffectency disseases

A

Retts syndrome

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31
Q

Oligodendrocytes mylonate the

A

CNS

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32
Q

Node is filled with

A

specific protiens
Na chnnels important for AP

Para node - cells interact with membrane (axon) itself - connecting two processes

also juxtaparanode

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33
Q

Oligodenrocyltes precurosr cell makes

A

olig progen cell
differentate into immature/premylanting olig

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34
Q

mylanating olig procues

A

mylen sheath that wraps around the acon

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35
Q

Nodes of Ranvere

A

area between two mylen sheaths

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36
Q

motor learning required

A

olig

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37
Q

MYRF

A

produce new mylen
genetic mutant only prevents new mylen - impared learning

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38
Q

how many mylen sheaths can one olig porduce

A

more than one for olig
only one for schawan cell

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39
Q

Negitives of mylenation and learning

A

continuously mynlating, cannot modulate neuons, take up unessary space

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40
Q

If Olig help in learning they cannot be

A

fully set/compleetly mylenating

(but mylen is esablshed at birth)

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41
Q

demylenation

A

not likely energy demand is too high

42
Q

How get olig so specificaly organize on axon

A

signalling
attractuve
repulsice (self avoidance)
Activity - responds to- and modulates

43
Q

MS is a __ disease

A

demylnating disease of the CNS

44
Q

Potental therapies on how to produce mylen sheaths

A
  1. take existing olig and express more mylen seaths - not likely - only a few hours to do in vivo
  2. make new olig, more likely
45
Q

Olig. Reside in the

A

CNS

46
Q

Olig Precursor directly make

A

Olig progen cell

47
Q

Olig organize in the nervous system with

A

proliforation, directonal migration, contat mediated repulsion

48
Q

SYG-1 functions in

A

neurons (SYG-2 is in vulval epiphelial cells)

49
Q

Functions of olig

A

main mylenating cell in the CNS
behavior, speed, provides nutrients

50
Q

generation of mylen seeth

A

Presursor (self renew)
Progen (self renew)
pre mylenating olig
mylenating olig - makes mylen seeths

51
Q

Can you have non-myelinating Olig?

A

No, can only have pre mylenating

52
Q

PNM domain produces

A

Olig and motor neurons (mainly)

53
Q

SHH gradient sets up

A

domains in the spinal cord

54
Q

DBX domain

A

produces olig

55
Q

how do olig set up in spinal cord

A

olig grow in DBX domain
PNM domain expresses olig 2 (#1 FT in olig., factors help drive defenteration, then drive migration)

56
Q

olig migrade as

A

progenetors,
contact neurons, upregulate mylen producing pathways

57
Q

Neural devolopment waves

A
  1. Neurons
  2. Astrocytes (new litature says may be first)
  3. Olig
  4. Later populations of neurons (ex. IN)
58
Q

MBP

A

myelin basic protein

59
Q

NG2

A

imature

60
Q

Olig “wars” dbx1

A

is higher up - also produce olig.

61
Q

gleogenisis

A

produce glial (not neurogenisis)

62
Q

motor neuron devolopment and olig arise from

A

distinct cell linages by progenetor recrutment

MN stays in PNM domain but moves outward (in PNM - olig 1 and olig 2 - PNM progen - motor neuron than olig but mainly motor)

olig decend from DBX domain (dorsal to ventral) and initates olig 2 expression, blocked by SHH (also blocking olig formation)

MN causes switch from SHH recurutment to PNM

63
Q

Scientist in Olig. Differentation (change by MN for olig to switch from SHH to PNM recruitment)

A

Bruce Apple

trained many women in the field including Sarah K

64
Q

Mozech animal

A

have two animal cells and lable one and put that cell into the animal to track those cells

65
Q

Old vs New model in olig formation

A

Old model -> precursor common cell -> MN & Olig

New model ->
Precursor 1 -> MN
Precursor 2 -> Olig

66
Q

Fait mapping

A

with photoconversion
express protine in PNM pro than change green to red (early on all green - not come from cell that express olig 2, olig 2 negative than become more ventral then become olig 2 positive)

67
Q

Olig are directly produced in the spinal cord from

A

PNM domain

68
Q

Olig and MN come from

A

Distinct progentors

69
Q

olig are directly produced from

A

olig progen cells

70
Q

SHH is a

A

videogame charator, also required in neurogenisis

71
Q

Schwan cell is the

A

mylenating cell of the PNS

72
Q

Schwan cell can be

A

mylenating (mature) and non mylenating (mature)

73
Q

Production and wraping of mylen sheeths

A

Schw pre produce -> Schw pro -> Pre mylenating Schw -> going to mylen

mylen seeths warp around -> gap between two sheeths, inner toung is wraped last

74
Q

Why study neural crest

A

occour later in devolopment from differnt germ layers

75
Q

Schw cells are produced from

A

neural crest cells

76
Q

Steps of how neural crest cells migrate

A
  1. move ventraly via ligands
  2. cell surface on axion “binds”
  3. moves along axon via triggering TFs
77
Q

Neural crest cells pre/pro gen vs once arive at axon

A

pre/pro gen -> pluripotant
at axon -> mylenation (main role, saltatory conductance)

78
Q

Olig vs Schw

A

Olig - multiple mylen on multiple axons, orgin CNS, larger nucleous not “on” axion

Schw - one mylen on one axon, orgin PNS/Neural crest, can be non mylenating

79
Q

How do Schw wrap around itself

A
80
Q

Critical period

A

morphology no longer changes

81
Q

Reconition of axion

A

mylenation is specific
both pos and neg cues

82
Q

two main signals that tell to mylenate

A

axion calliber - size of axion (diameter)

and activity

83
Q

two hyposises for size of axon and mylnation

A
  1. molecular cues reading sixe
  2. symple physics/size promotes more rings

determined by wraping around something that isnt an axion (nanofiber) which also shows size dtermining mylenation ammount (proving theroy #2)

however there are cues in addition to axon caliber

84
Q

activity and mylenation

A

not all or nothing but is am “I” more active than neghbors (if more than normal but has a very active neghbor= both have same mylenation)

activity is also important in length of mylen seeth not just number of seeths

85
Q

paranodal bridges

A

make new seeths

86
Q

Schwann cells reside in

A

PNS
sensory and motor systems
Autonomic
Sympathetic

87
Q

Nueral crest cells do not produce

A

Olig. (do produce pigment cells, sensory neurons, schwann cells)

88
Q

Olig are distinct from schwann because they

A

can wrap multiple axions

89
Q

__ have been shown to control mylenation

A

activity and acon calilber

90
Q

Wraping of sheeths is ___ in nature

A

quantanary
as time goes on - steps down in brigness sugesting iddle is where leading edge is

91
Q

liquid croissant model of mylenation

A

“triangular pice” wraps than folds/flattens out.

92
Q

New layer of mylen is awlays

A

closest to the axion

93
Q

inner tough ____ pushing foward

A

action dinamics, cytoskelition re arrangments (in inner toung)

94
Q

___ facilates compaction

A

MBP

95
Q

“attach to axion”

A

ends of mylen loops in para node and juxtaparanode

96
Q

highly structured node

A

Nav1 (Na channel) -within node
Casor (involved in adhesion) - attractions mylen loops
Kv1 (K channel) - juxtaparanode

97
Q

most mylenation is not

A

till birth

98
Q

mylen is plastic via

A

making new sheets
repacing old with new
changing thickness
inc. length
inc. closeness

99
Q

Chaecot-Marie-Tooth dieases

A

in PNS starts with most distal musles
caused by two types of disfunctions - demylantion and acional degrdation

100
Q

gpr 126 drives

A

differnatino of promylenating shwann cells by inc cAMP - triggerning oct6 expression (and krox 20) and mylenation

101
Q

gpr 126 is req for mbp in

A

PNS only

NeuroBiology (9 decks)

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