Topic 1 Flashcards
Neurons
10% of cells in brain
process information
sensing environment
signal transmission
Glia
Support Neurons
immune cells of the brain
Types of Glia
Astrocytes
Ependymal
Oligodendroctyes
Microglia
Astrocyte function
A for Abundant
support and nourish electrons - scaffold the brain
Regulate the chemical content of extracellular space - by regulating substances that affect neurotransmitter
have end feet - at the end of synapses that
fill in spaces between proteins
Microglia function
Immune cells of the brain
Remove threats + clean debris
Oligodendrocytes
Myelinating cells of the CNS
one oligodendrocytes myelinate many axons
Ependymal
Makeup lining of ventricles and spinal cord
produce and circulate cerebrospinal fluid
Cytoarchitecture
Celluar structure of the brain
Golgi Stain
Staining individual neurons within the brain
Breakthrough in neurology
Neurite
A projection from the cell body
2 types - axon and dendrited
Nissil Granules
Found in Soma (cell body)
Synthesis proteins
Have a rough ER
Neurotubules
Is the cytoskeleton in neurons
Axonplamsa
Cytoplasm in the axon hillock
Nodes of Ranvier
Gaps in between myelin sheaths
AP occur in these region, AP can doesn’t occur in myelinated sections
Salatory Conduction
AP jumping from node of Ranvier to node of Ranvier
Types of synapses
Axoaxonal
Axodendritic
axosomatic
Axoplasmic Trasnport
Axon contains microtubules
these microtubules transport proteins down the axon
Antretrograde transport
Transport from the cell body to the terminal
Retrograde Transport
Transport from the synapse to the soma
Neuronal Classification
Classified based on number of neurites
Unipolar
bipolar
multipolar
Stellate
Star shaped classification
Pyramidal
shape classification
Asymmetrical
Long axon
short dendrite
Looks like a pyramid
Golgi type 1
axon length classification
have a long axon
Golgi type 2
Axon classification
short axons
synapse with other axons locally
Classified based on structure
Motor neurons
sensory neurons
interneurons
Classified based on Neurtransmitter
dopaminergic neurons relase dopamine
GABAergic neurons relase GABA
Glutamatergic neurons release glutamate
Schwann Cells
myelinate neurons in the PNS
1 Schwann cell: 1 axon
Oligodendrocytes
Myelinating cells of the CNS
wrap around the axon
1 oligo: numerous axons
insulates, nourishes and protects axon
allows for salatory conduction
Inhibit axonal regrowth
Increases speed of AP
Microglia
constanly moving in brain montioring for pathogens or cells that may be a threat
when activated they morph into phagocytes to exterminate
Structure of Myelin
Oligodenrties have spinal structure
allows membrane to wrap around axon
creates a multilayered structure
Satelite cells
Astrocytes of the PNS
Nodes of ranvier
Allows for saltatory conduction
ensures AP is completely regenerated before firing a new AP
Proteins in myelin
Very low protein count - as it has more lipids to allow for insulation
MBP
Myelin basic protein
most common
ensures cell is tightly wrapped around neuron
also keeps cytoplasmic surface close to myelin
PLP
Proteolipid Protein
helps myeline structure
without degradation occurred
OSP
Oligodendrocyte specfic protein
tight junction protein
MAG
protein with a carb in it
involved with neuron - oligodendrocyte interaction
How did they discover Myelin proteins
Genetically engineered rats by removing the gene that codes for the protein, once removed they monitored the symptoms
Without PLP
structural abnormailities but still compact
Without BMP
poor compaction, degradation
Demylination
Loss of structurally sound myelin
can occur due to exposure to harmful substances, i.e lead
Primary demylination
Type of demyelination
when the myelin sheath is lost but the axon underneath is fine
Axonal damage
Type of demyelination
when the sheath is lost and the axon is damaged
Dysmyelination
When the myelin wasn’t formed correctly in the first place - usally a genetic mutation
Remyelination
The capacity of myelin to regenerate
each time it regenerates it won’t be the same, usually worse
usally caused by an inflammatory response
common during early stages of MS
Leukodystrophine
Disorders affecting the myelin sheath
all genetic and extremely rare
i.e Krabbs, pelizaues-mertzbacher, adrenoleukodystrophy
Multiple Sclerosis
demyelination caused by an auto-immune response, exact cause is unknown
age of onset - 18 - 50
MS symptoms
Numbness and tingling in legs, arms, face
muscle weakness, blurred vision, extreme tiredness, speech problems
Clinically Isolated syndrome
when symptoms only appear for 24 hours
Monofocal
only affect one region of the brain resulting in one symptom
Mulitfocal
Affects multiple reigons of the brain - causing multiple symptoms
How MS happens
T cells with a special ligand are able to break through the blood-brain barrier
this allows more receptors to follow suit, like paying the bouncer to let your friends in, i.e lets b cells and other cytotoxins in
B-cells bind to myelin causing macrophages to attack then t-cells stop it and remyelination occurs
Relapsing-Remitting MS
85% are diagnosed with this
attack - gets better and regenerates - relapse occurs and regenerates again but regeneration is never fully completely
very slow progression of sympotms
Secondary Progressive MS
Starts as RRMS but then the remission period stops and then there is just a gradual prgoression
Primary progressive MS
No remission
Just a gradual progression
Progressive relapsing (PRMS)
Is primary progressive but with remission peroids, Like RRMS except occurs linealry
Charcot’s Neurlogic Triad
Symptoms of MS
Dysarthria
Nystagmia
International tremors
Dysarthia
Difficult or unclear speech
occurs when there is plaque in the brainstem
Nystagmia
Involuntary rapid eye movements
caused by plaque forming on the nreves of the eyes
also causes loss of vision, double vision
Intenetion tremors
caused by plaque forming on motor neurons
causes muscle weakness and fatigue
Lhermitte’s Sign
when patient bends neck forward, an electric shock radiates down their back and into their limbs
MS diagnosis
MRI scan, visual evoked potential test (shows delayed AP), cerebrospinal fluid - high levels of antibodies
MS treatment
No cure, give immunosurpressents or corticosteroids (they rebalance amount of inflammatory agents int the brain)
plasmapheresis
MS prognosis
no cure, just keep giving medication and monitor symptoms
Gullian Barr syndrome
demyelination in PNS
starts as tingling or paraylsis in feet and ascends
can progress to respiratory or heart failure
is bilateral
appears after a GIT or respiratory infection
poly neuropathy
damage to PNS nerves
AIDP
Acute inflammatory demylination polyneuropathy - type of GBS
AMAN
Acute motor axonal neuropathy
attacks nodes of ranvier - decreases conduction velocity
Molecular mimicing
Antigens from a previous infection to ones already found in the body , they attach to the axon and macrophages attack them ruining the neuron during the process
GBS diagnosis
No specific test can be conducted
knee jerk reflex will be absent
electromyography - measures electrical activity of muscles - will be reduced
GBS treatment
Mostly supportive
corticosteroids or immunosuppressant - both reduce activity of the inflammatory and immune response
plasmaphoresis
acute phase
GBS phase
firstly couple weeks
symptoms occur and worsen
plateu phase
symptoms remain but dont worsen
return phase
remyelination occurs
phases of GBS
acute phase, plateau phase and return phase
PNS remyelination
can occur if axon is still intact
occurs very very slowly as it is a complex process
