PKCγ promotes axonal remodeling in the cortico-spinal tract via GSK3β/β-catenin signaling after traumatic brain injury

Scientific Reports, 2019 · DOI: 10.1038/s41598-019-53225-y · Published: November 19, 2019

Simple Explanation

Traumatic brain injury (TBI) can cause lasting motor deficits. This study explores how a protein called PKCγ affects nerve fiber regrowth after TBI. The researchers found that PKCγ promotes the growth of nerve fibers from the uninjured side of the brain to the injured side, helping to restore motor function. Activating PKCγ could be a new way to help people recover from TBI by encouraging the brain to rewire itself.

Study Duration

5 weeks

Participants

BALB/c mice

Evidence Level

Not specified

Key Findings

1
PKCγ is activated in the corticospinal tract (CST) on the uninjured side of the brain after TBI, suggesting it plays a role in the brain's response to injury.
2
Activating PKCγ promotes the growth of new nerve fibers and branches, but not the extension of existing fibers.
3
PKCγ promotes axonal outgrowth by stabilizing β-catenin, a protein involved in cell growth and development.

Research Summary

This study investigates the role of PKCγ in axonal remodeling after traumatic brain injury (TBI). The research demonstrates that PKCγ promotes neuronal differentiation and axonal outgrowth, contributing to functional recovery after TBI in mice. The findings suggest that PKCγ could be a potential therapeutic target for enhancing brain repair and functional recovery following TBI.

Practical Implications

Therapeutic Target

PKCγ may be a potential therapeutic target for physiological and functional repair after TBI.

Drug Development

Drugs that activate PKCγ could enhance midline crossing and functional recovery in TBI patients.

Rehabilitation Strategies

Understanding the role of PKCγ can help in developing more effective rehabilitation strategies.

Study Limitations

1
The study lacks characterization of PKCγ-signal mediated gene target alterations, particularly Wnt/β-catenin and GAP43 targets.
2
The underlying mechanism of PKCγ activation and the polarity of midline crossing characterization after TBI has not been fully understood.
3
The possibility that the compensation derived from TBI induced intrinsic signaling cannot be excluded.

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