Exam 2 Flashcards
Synapse
Physical connection of two neurons that transfer neuronal information from one to the other
Pre synaptic
part of synapse sending the info
post synaptic
part of synapse recieving the info
Snaptogenesis
formation of synapses
Snaptic specificity
formation of correct and not incorrect synapseds
PSD
post snaptic density
NT receptors and number of protens - helps modulate
Mitochondria in presnaptic
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)
Neurotransmiter transporters
reuptake (if not would stay in cleft and bind causing AP)
Snaptic vessicels
some with NT in it - fuse with membrane
Chemical synapses
clear structural difference between pre and post synaptic
chemical elicit comunication
primaraly in nervous system (slower)
easier to see - easier to study
Electrical synapses
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
types of chemical synapses
excitatory and inhibitory
Vesicle binding to target plasma membrane
protein targets on vesicle and membrane
zippering of proteins (if inhibit this than inhibit NT from releasing)
Why spontanious relese of NT/ vessicles
need to be primed for when needed it (so would not want to completely shut of ever, would want to modulate)
spontaious relese
vessicle relase NT not in secronized fassion
Patch clamp
suck up part of membrane
Need for reflux reaction
exitatory neusons and inhibitoyu neurons (so not sence heat once move off)
ionotropic receptor
assocated with actual firing event
on or off
metabatropic receptor
modulate ion changels
sould be this much on or this much off
Ach (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)
Exitatory
Alz
Dopamine (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)
Inhibitory
Parkinsins
Serotonin (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)
Inhibitory
depression, mood disorders
Norepinephrine (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)
Excitatory
mental disorders, depression
GABA (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)
Inhibioty
anxiety
Endorphins (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)
Inhibitory
body experences pain
Glutamate (Function, Effect of Deficit, Effect of Surplus, Agonist, antagonist)
exitatory
(seesures?)
Steps of Synaptogenesis
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
Synaptic specificity is generated by
the synaptic guidepost protein SYG2 and its receptor SYG1
Why does the nervous system need glial cells
speed, saltatory conduction, nodes of Ranveer
microglia deffectency disseases
Retts syndrome
Oligodendrocytes mylonate the
CNS
Node is filled with
specific protiens
Na chnnels important for AP
Para node - cells interact with membrane (axon) itself - connecting two processes
also juxtaparanode
Oligodenrocyltes precurosr cell makes
olig progen cell
differentate into immature/premylanting olig
mylanating olig procues
mylen sheath that wraps around the acon
Nodes of Ranvere
area between two mylen sheaths
motor learning required
olig
MYRF
produce new mylen
genetic mutant only prevents new mylen - impared learning
how many mylen sheaths can one olig porduce
more than one for olig
only one for schawan cell
Negitives of mylenation and learning
continuously mynlating, cannot modulate neuons, take up unessary space
If Olig help in learning they cannot be
fully set/compleetly mylenating
(but mylen is esablshed at birth)
demylenation
not likely energy demand is too high
How get olig so specificaly organize on axon
signalling
attractuve
repulsice (self avoidance)
Activity - responds to- and modulates
MS is a __ disease
demylnating disease of the CNS
Potental therapies on how to produce mylen sheaths
- take existing olig and express more mylen seaths - not likely - only a few hours to do in vivo
- make new olig, more likely
Olig. Reside in the
CNS
Olig Precursor directly make
Olig progen cell
Olig organize in the nervous system with
proliforation, directonal migration, contat mediated repulsion
SYG-1 functions in
neurons (SYG-2 is in vulval epiphelial cells)
Functions of olig
main mylenating cell in the CNS
behavior, speed, provides nutrients
generation of mylen seeth
Presursor (self renew)
Progen (self renew)
pre mylenating olig
mylenating olig - makes mylen seeths
Can you have non-myelinating Olig?
No, can only have pre mylenating
PNM domain produces
Olig and motor neurons (mainly)
SHH gradient sets up
domains in the spinal cord
DBX domain
produces olig
how do olig set up in spinal cord
olig grow in DBX domain
PNM domain expresses olig 2 (#1 FT in olig., factors help drive defenteration, then drive migration)
olig migrade as
progenetors,
contact neurons, upregulate mylen producing pathways
Neural devolopment waves
- Neurons
- Astrocytes (new litature says may be first)
- Olig
- Later populations of neurons (ex. IN)
MBP
myelin basic protein
NG2
imature
Olig “wars” dbx1
is higher up - also produce olig.
gleogenisis
produce glial (not neurogenisis)
motor neuron devolopment and olig arise from
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
Scientist in Olig. Differentation (change by MN for olig to switch from SHH to PNM recruitment)
Bruce Apple
trained many women in the field including Sarah K
Mozech animal
have two animal cells and lable one and put that cell into the animal to track those cells
Old vs New model in olig formation
Old model -> precursor common cell -> MN & Olig
New model ->
Precursor 1 -> MN
Precursor 2 -> Olig
Fait mapping
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)
Olig are directly produced in the spinal cord from
PNM domain
Olig and MN come from
Distinct progentors
olig are directly produced from
olig progen cells
SHH is a
videogame charator, also required in neurogenisis
Schwan cell is the
mylenating cell of the PNS
Schwan cell can be
mylenating (mature) and non mylenating (mature)
Production and wraping of mylen sheeths
Schw pre produce -> Schw pro -> Pre mylenating Schw -> going to mylen
mylen seeths warp around -> gap between two sheeths, inner toung is wraped last
Why study neural crest
occour later in devolopment from differnt germ layers
Schw cells are produced from
neural crest cells
Steps of how neural crest cells migrate
- move ventraly via ligands
- cell surface on axion “binds”
- moves along axon via triggering TFs
Neural crest cells pre/pro gen vs once arive at axon
pre/pro gen -> pluripotant
at axon -> mylenation (main role, saltatory conductance)
Olig vs Schw
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
How do Schw wrap around itself
Critical period
morphology no longer changes
Reconition of axion
mylenation is specific
both pos and neg cues
two main signals that tell to mylenate
axion calliber - size of axion (diameter)
and activity
two hyposises for size of axon and mylnation
- molecular cues reading sixe
- 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
activity and mylenation
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
paranodal bridges
make new seeths
Schwann cells reside in
PNS
sensory and motor systems
Autonomic
Sympathetic
Nueral crest cells do not produce
Olig. (do produce pigment cells, sensory neurons, schwann cells)
Olig are distinct from schwann because they
can wrap multiple axions
__ have been shown to control mylenation
activity and acon calilber
Wraping of sheeths is ___ in nature
quantanary
as time goes on - steps down in brigness sugesting iddle is where leading edge is
liquid croissant model of mylenation
“triangular pice” wraps than folds/flattens out.
New layer of mylen is awlays
closest to the axion
inner tough ____ pushing foward
action dinamics, cytoskelition re arrangments (in inner toung)
___ facilates compaction
MBP
“attach to axion”
ends of mylen loops in para node and juxtaparanode
highly structured node
Nav1 (Na channel) -within node
Casor (involved in adhesion) - attractions mylen loops
Kv1 (K channel) - juxtaparanode
most mylenation is not
till birth
mylen is plastic via
making new sheets
repacing old with new
changing thickness
inc. length
inc. closeness
Chaecot-Marie-Tooth dieases
in PNS starts with most distal musles
caused by two types of disfunctions - demylantion and acional degrdation
gpr 126 drives
differnatino of promylenating shwann cells by inc cAMP - triggerning oct6 expression (and krox 20) and mylenation
gpr 126 is req for mbp in
PNS only
