Trigger 7: Microglia Flashcards
(33 cards)
TBI results in neuroinflammation which include activation of
local ramified microglia- amoeboid shape- which leads to the production of inflammatory cytokines
which substances leak out of the brain during TBI
a huge efflux of …
glutamate
chloride
potassium and sodium
swelling and inflammation from tissue damage
increase the pressure, producing more damage
when swelling and inflammation from tissue damage occurs
♣ a craniotomy is performed to prevent pressure cuaisng more damage
♣ NO KNOWN DRUG WHICH STOPS THIS
♣ No treatment which stops leakage of NT
positives of inflammation
necessary for clearance of harmful substance (cell debris) after TBI
negatives of inflammation
contributes to brain injury following TBI
microglia are the
resident macrophages of the brain- helping to maintain homeostasis by removing debris and toxic substances
after trauma
microglia are activated promptly morning into a motile amoeboid state and migrating to damage regions
microglia have been found to have two polarisation states
M1 and M2
M1 activated by
LPS, IFN-Y, TNF-a
M1 release
TNF-a, IFN-y, iNOS, IL-1B, IL-6
M2 activated by
IL4, IL-13, IL-10, TGF-B
M2 release
TGF-B, arginase 1, Ym1, FIZZi, IL-10
M2 play a role in
- resolution of neuroinflamamtion
- clearance of debris
- CNS remodelling and neuronal repair
- neurogenesis and angiogenesis
oligodendrocyte differentiation
demyelination
microgliosis
Where microglia in a resting state become activated. - –Microglial cells are the primary initiators of the central inflammatory response to acute and chronic disorders.
outline microliosis process
1) ramified microglia carrying out immune surveillance
2) TBI injury
3) activation of microglia –> M1 and M2
4) if resolved microglia return to resting state
4) if unresolved the microglia become primed with increased MHCII and CD68
5) microglia become hyperacitvation e.g. by immune challenge
6) release of inflammatory markers
M1 can lead the production of
free radical generation
free radicals cause
mitochondrial dysfunction–> accelerated excitotoxicity and synaptic dysfunction
–> immunoexcitoxicity
astrogliosis
Astrogliosisis an abnormal increase in the number of astrocytes due to the destruction of nearby neurons from CNS trauma, infection, ischemia, stroke, autoimmune responses, and neurodegenerative disease
result of astrogliosis
glial scar formation
astorgliosis process
1) healthy astrocyte activated due to TBI/ insult
2) astrocyte becomes a reactive astrocyte (proliferate and migrate
3) which are recruited to the site of injury
4) goal scar
the scar secretes
neuro-developmental inhibitor molecules - preventing couple physical and functional recovery of the CNS after insult
intracellular molecular cascade by astrogliosis
look at notes
