Interactive image analysis programs for quantifying injury-induced axonal beading and microtubule disruption

Kilinc, Devrim; Gallo, Gianluca; Barbee, Kenneth A.

doi:10.1016/j.cmpb.2009.01.002

Cited by 16 publications

(9 citation statements)

References 23 publications

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“…Images were obtained immediately after and 60–90 min after the injury. To quantify axonal beading, we used a Matlab-based (MathWorks, Natick, MA) interactive image analysis program that successfully detects axonal beading(Kilinc et al, 2009). The beading score is the volume-weighted sum of the radii of axonal swellings, whose diameter was at least twice the axon diameter, normalized by the length of the axon in question.…”

Section: Methodsmentioning

confidence: 99%

Mechanical membrane injury induces axonal beading through localized activation of calpain

Kilinc

Gallo

Barbee

2009

Experimental Neurology

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Diffuse axonal injury (DAI), a major component of traumatic brain injury, is characterized by a sequence of neurochemical reactions initiated at the time of trauma and resulting in axonal degeneration and cell death. Calcium influx through mechanically induced axolemmal pores and subsequent activation of calpains are thought to be responsible for the cytoskeletal damage leading to impaired axonal transport. Focal disruption of cytoskeleton accompanied by the accumulation of transported membranous cargo leads to axonal beading which is the characteristic morphology of DAI. By applying fluid shear stress injury on cultured primary neurons, acute calcium (Ca 2+ ) and calpain responses of axons to mechanical trauma were investigated. Intracellular Ca 2+ concentration ([Ca 2+ ] i ) shows a steady increase following injury that can be blocked by sealing membrane pores with Poloxamer 188 and by chelating intra-or extracellular Ca 2+ . Calpain activity increases in response to mechanical injury and this increase depends on Ca 2+ availability and on axolemmal permeability. Both the [Ca 2+ ] i increase and calpain activity exhibit focal peaks along the axons which co-localize with mitochondria and predict future axonal bead locations. These findings suggest that mechanoporation may be the initiating mechanism resulting in ensuing calcium fluxes and subsequent calpain activity and that post-injury membrane repair may be a valid therapeutic approach for acute intervention in DAI.

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Section: Methodsmentioning

confidence: 99%

Mechanical membrane injury induces axonal beading through localized activation of calpain

Kilinc

Gallo

Barbee

2009

Experimental Neurology

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“…Understanding the mechanisms leading to such a shape transformation is of major importance since, for instance, axonal beading is triggered by mechanical trauma (Kilinc et al, 2008(Kilinc et al, , 2009Hemphill et al, 2015;Goriely et al, 2015;Lang et al, 2017), and is also believed to precede axonal atrophy in Alzheimer's disease, Parkinson's disease, and other neurodegenerative conditions (Datar et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Necking, beading, and bulging in soft elastic cylinders

Jin

Goriely

2021

Journal of the Mechanics and Physics of Solids

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“…The well-known peristaltic instability in which soft slender cylinders/tubes adopt axisymmetric beads under bulk and surface stresses has drawn much attention in recent years [18][19][20][21][22][23]. This bifurcation phenomenon can occur in stretched nerve fibres [24], in axons under mechanical trauma [25,26], and it has also been implicated in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases [27]. Also, stretched tubes termed tunnelling nanotubes have been observed between migrating cells, and allow for inter-cellular communications and migration support [28][29][30][31][32][33].…”

Section: Introductionmentioning

confidence: 99%

Post-bifurcation behaviour of elasto-capillary necking and bulging in soft tubes

Emery

2021

Proc. R. Soc. A.

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Previous linear bifurcation analyses have evidenced that an axially stretched soft cylindrical tube may develop an infinite-wavelength (localized) instability when one or both of its lateral surfaces are under sufficient surface tension. Phase transition interpretations have also highlighted that the tube admits a final evolved ‘two-phase’ state. How the localized instability initiates and evolves into the final ‘two-phase’ state is still a matter of contention, and this is the focus of the current study. Through a weakly nonlinear analysis conducted for a general material model, the initial sub-critical bifurcation solution is found to be localized bulging or necking depending on whether the axial stretch is greater or less than a certain threshold value. At this threshold value, an exceptionally super-critical kink-wave solution arises in place of localization. A thorough interpretation of the anticipated post-bifurcation behaviour based on our theoretical results is also given, and this is supported by finite-element method simulations.

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Interactive image analysis programs for quantifying injury-induced axonal beading and microtubule disruption

Cited by 16 publications

References 23 publications

Mechanical membrane injury induces axonal beading through localized activation of calpain

Mechanical membrane injury induces axonal beading through localized activation of calpain

Necking, beading, and bulging in soft elastic cylinders

Post-bifurcation behaviour of elasto-capillary necking and bulging in soft tubes

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