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Slide 1 This presentation is about the summary of
two papers related with Axotomy, which means the
neuronal axon transection.
Slide 2 First paper is “Laser-based single axon
transection for high-content axon injury and regeneration
studies” published in PLoS One on 2011, And Second is “Axotomy depletes intracellular
calcium stores in primary sensory neurons” published
in Anesthesiology on 2009.
Slide 3 In the first paper, researchers studied the
retinal neuronal RGC-5 cell line after laser transection for
demonstrating that the ability of these cells to initiate a regenerative response correlates
with axon length and cell motility after injury.
They used the low energy picosecond pulsed laser with
7nJ pulse energy, 5s exposure duration, 1064nm wavelength and 6ps pulse width for axotomy.
Slide 4 Firstly, they distinguished three groups of
RGC-5 cells based on morphological responses to
axonal injury, whether they initially regenerated their transected axon. Group A is cells either
re- sealed the injured axonal membrane and reversed
axon transection, reconnected the transected sections or grew new processes at the damage
site. Group B is cells that neither repaired nor
replaced their injured axons and Group C is injured cells died within one day of injury.
There were two different features related with regeneration
between these three groups, Cell body motility and axon length. Results indicate that Cells
which regenerated their axons had a lower mean
motility than cells that did not, and cells with longer axons were less likely to initiate
a regenerative program after axotomy compared
with those with shorter axons.
Slide5 Next in second paper, researchers examined
the effect of injury on intracellular calcium ion stores
of the endoplasmic reticulum, which critically regulate the calcium signal and neuronal function.
Endoplasmic reticulum calcium ion stores released by the ryanodine-receptor agonist caffeine
decreased by 46% in axotomized small neurons. Thies effect persisted in Calcium ion-free
bath solution which removes the contribution of
store-operated membrane calcium channels, and after
blockade of the mitochondrial, sarco-endoplasmic calcium-ATPase and the plasma membrane
calcium ATPase pathways.
Slide 6 Calcium ion released by the sarco-endoplasmic
calcium-ATPase blocker thapsigargin and by the
calcium-ionophore ionomycin was also diminished by 25% and 41%.
Slide 7 In contrast to control neurons, calcium ion
stores in axotomized neurons were not expanded by
neuronal activation by potassium depolarization, and the proportionate rate of refilling by
sarco- endoplasmic calcium-ATPase was normal. Luminal
calcium concentration was also reduced by 38%
in axotomized neurons in permeabilized neurons.
Slide 8 In summary, First article indicates that RGC-5
cell motility was related to the level of injury and
the liberation of chemoattractant molecules from the injury site depend on the injury
level, and Second article show that the amount of calcium
ion which can be released from stores through a
variety of pathways is diminished after axotomy.