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In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
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Concussive Head Trauma Deranges Axon Initial Segment Function in Axotomized and Intact Layer 5 Pyramidal Neurons.

Alan C Harris1, Jianli Sun2, Kimberle M Jacobs1

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|August 31, 2023
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Summary
This summary is machine-generated.

Traumatic brain injury disrupts the axon initial segment (AIS), impairing neuron function. Mitochondrial calcium dysregulation contributes to this AIS dysfunction after injury.

Keywords:
adult brain injuryaxonal injuryconfocal microscopyelectrophysiologytraumatic brain injury

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Area of Science:

  • Neuroscience
  • Cell Biology

Background:

  • The axon initial segment (AIS) is crucial for action potential (AP) generation and neuronal signaling.
  • Neocortical axonal injury, common in traumatic brain injury (TBI), often occurs at the AIS, potentially disrupting its specialized function.

Purpose of the Study:

  • To investigate how concussive TBI affects the functional specialization of the AIS.
  • To identify the cellular mechanisms underlying AIS dysfunction post-TBI.

Main Methods:

  • High-resolution recordings of APs from layer 5 pyramidal neurons in Thy1-YFP-H mice one and two days after mild central fluid percussion injury.
  • Second derivative (2°) analysis to quantify AIS- and soma-regional contributions to the AP upstroke.
  • Assessment of AIS morphology and excitability, including ankyrin-G staining.

Main Results:

  • A subset of axotomized neurons showed an abolished AIS-regional 2° peak, indicating functional perturbation, diminished excitability, and AIS distention.
  • Another subpopulation exhibited merged AIS- and soma-regional 2° peaks, suggesting altered sodium channel function or AIS initiation zone translocation.
  • Knockout of cyclophilin-D ameliorated these effects, implicating mitochondrial calcium dysregulation.

Conclusions:

  • Concussive TBI causes significant functional and structural perturbations of the AIS.
  • Mitochondrial calcium dysregulation is a key factor in trauma-induced AIS dysfunction.
  • These findings highlight the AIS as a vulnerable site in TBI and suggest potential therapeutic targets.