Neuro Exam 4.12
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Neuro Exam 4.12
neurology neuroscience neuroanatomy
review of neuro part 12 for exam 4
Degree of regeneration of the NS will:
Is the PNS successful in regeneration?
What makes up the PNS?
CNs and spinal nn
both motor or sensory (or mixed)
What surrounds the peripheral nerve in the PNS?
What surrounds the vesicles in the PNS?
What surrounds each axon in the PNS?
endoneurium (endoneurium tube) which is connective tissue
Review Anatomy of Peripheral Nerve
see section 1
Is the CNS successful in regeneration?
not very successful
replacement of cells or tissue w/ identical cells or tissue (occurs if cell body is not harmed)
replacement of living cells or tissue w/ cells or tissue of a more primitive nature (like scar tissue) --it is not the same
Do we want regeneration or repair?
regeneration (we don't want scar tissue from repair)
When can neurons regenerate?
after any kind of trauma or disease process
What will vary after the injury?
Why does functional success vary after the injury?
depends on location of damage
Regeneration is generally successful in the ___, not the ___.
PNS, not the CNS
What happens if you damage the motor neurons in the PNS?
What happens if you damage the sensory neurons in the PNS?
loss of general sensation
A transected peripheral N will cut what?
motor and sensory properties
When can regeneration occur in the PNS?
if the cell body is not permanently damaged
Can regeneration occur in PNS or CNS if the cell body is damaged?
When does Wallerian degeneration occur?
after a lesion in peripheral nerve
Which part of a neuron undergoes Wallerian degeneration?
axon distal to lesion
predictive, degenerative series
Schwann cells on distal portion degenerate over a longer time
In Wallerian degeneration, what happens to everything distal to the cut?
degenerates in predictable manner
-Schwann cells (take longer)
What is the inflammatory process from Wallerian degeneration?
What happens to the endoneurium (endoneurial tube) during Wallerian degeneration?
stays in place (up to 30 days after initial injury) despite degeneration of axons and Schwann cells
What do axons form during Wallerian degeneration?
filopoda (distal end) at the area of the lesion
What do the filopoda make up?
What does one filopoda become?
What happens to all filopoda besides the dominant extension?
What does the dominant extension do?
enters and grows down endoneurial tube to target structure
What facilitates growth of the dominant extension?
NGF produced by target structures and Schwann cells
Do Schwann cells remyelinate down the endoneurial tube?
CNS oligodendrocytes -> 1st order sensory neuron -> Schwann Cells (NGF, BDNF, Neurotrophins) ->
target recognition signals from target cells (NG, BDNF, Neurotrophins)
Rate of regeneration is variable based on:
area of the body
How fast does the upper forearm regenerate?
How fast does the distal forearm regenerate?
How fast does the wrist and hand regenerate?
What can we predict from the different rates of regeneration at different parts of the body?
estimate how many months regeneration will take
What determines the success of regeneration in PNS?
depends on type of injury
length of time b/w injury and repair work by surgeon
general nutritional status and health of individual affected (health good then heals better)
What are the possible types of nerve injury?
Which type of injury has an easier time regenerating?
endoneurial tubes are better preserved, they are only squished and the tube integrity is maintained
Transected (cut) injury:
interrupts integrity of the nn; there is an immediate inflammatory process w/ scar tissue
resultant environment is difficult for regenerating axons to get through debris
If you were naturally injured and you don't go to the dr. they will heal themselves overtime.
If you cut a nerve, you need surgical intervention
Where does regeneration of the CNS occur?
in brain and SC
Does mitosis occur in the CNS?
What part of the neuron gets damaged in the CNS?
What happens when axons are damaged in the CNS?
interferes w/ development of synapses b/w axons and dendrites (communication dependent or integrity of synapses)
What happens when neurons are damaged in the CNS?
very devastating damage
What was the belief about why the CNS can't regenerate?
thought to be an intrinsic characteristic of neruons themselves
What evidence is there to support that the inability to regenerate is not an intrinsic characteristic?
CNS neurons could regenerate in vitro if environment was conditioned; sut up artificial conditions in the living organism (vitro) and gave them the appropriate culture and they grew
same experiment was repeated with new techniques and definitely showed that CNS neurons can regenerate
If there is evidence against it, why don't neurons regenerate in the CNS?
there are CNS environmental characteristics which prevents significant regeneration as compared to regeneration in the PNS
the failure to regenerate is not an intrinsic characteristic of the neurons as previously thought
Recent research has shown that the oligodendrocytes produce inhibitory chemicals (NOGO factors), which prevent regeneration. Thus the problem is environmental, not genetic
What does the evidence imply?
there are no characteristics about the CNS environment that prevent significant regeneration as compared to regeneration in the PNS
the failure to regenerate is not due to intrinsic characteristics of the neurons as previously thought
So, what constitutes successful regeneration in the CNS?
multi-step process which includes the following:
-injured neuron must survive (cell body intact) [cells in cortex die, cell bodies die; cell in white matter will be ok b/c cell bodies are still intact]
-damaged axon must extend across the cut or damaged process to original neuronal target
once contract is made w/ target structures, axon needs to be remyelinated and functional synapses need to form on surface of target neurons
How can the criteria for successful regeneration in the CNS be evaluated?
: anatomical tracers--colored markers in growing axon (amino acids)
functionally (via physiological and behavioral outcomes)
: did they regain function? damage and then regenerated and function returns
What is the major problem w/ CNS research?
other compensatory mechanisms (neuroplasticity) need to be ruled out as the reason for increase in function
It is well established developmentally, that certain molecules (NGF, neurotrophins, etc) play a role in:
axon guidance and synaptogenesis
What type of influence do some of these molecules (that play a role in axon guidance and synaptogenesis)?
inhibitory (inform axons when to stop, turn right, go at an angle, etc)
Using monoclonal antibody techniques, inhibitory molecules in the adult CNS were shown to:
be produced by by the oligodendrocytes
What are the inhibitory molecules that play a role in axon guidance?
chemicals called NOGO factors
Are there other chemicals that do the same thing as NOGO factors?
molecules that inhibit the progression of axons
lie dormant under normal conditions
When CNS is damaged, what happens with NOGO?
there is an increase in NOGO production by oligodendrocytes
Why is NOGO a paradox?
following trauma, NOGO are produced to prevent regeneration in the traumatized area
normally, NOGO are used to suppress axons so you don't get too many
under normal conditions they are very important in initial development and under pathological conditions they are harmful
Research shows that these molecules (NOGO) are:
re-expressed after damage to CNS by oligodendrocytes
What is a research area concerning NOGO and CNS regeneration?
the focus of molecular intervention is to develop drugs which will inhibit the action of the inhibitory molecules so that regeneration and synaptogenesis can proceed