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  4. Effects of lipopolysaccharide-induced inflammation on expression of growth-associated genes by corticospinal neurons

Effects of lipopolysaccharide-induced inflammation on expression of growth-associated genes by corticospinal neurons

BMC Neuroscience, 2006 · DOI: 10.1186/1471-2202-7-8 · Published: January 24, 2006

Regenerative MedicineNeurologyGenetics

Simple Explanation

This study explores whether inflammation can promote nerve regeneration in corticospinal neurons, which usually don't regenerate well after spinal cord injury. The researchers applied lipopolysaccharide (LPS), a substance that causes inflammation, to the motor cortex of rats to see if it would stimulate these neurons to express genes associated with growth. The application of LPS induced inflammation in the motor cortex, leading to increased expression of certain growth-associated genes like c-Jun, SCG10, and GAP-43 in corticospinal neurons. However, it had limited effects on the expression of ATF3 in neurons, although glial cells in the subcortical white matter did show increased ATF3 expression. Despite the increased expression of growth-associated genes, the inflammation caused by LPS was not enough to promote the regeneration of the corticospinal tract after spinal cord injury. The corticospinal axons did not grow into or beyond the lesion site.

Study Duration
1 Day to 1 Month
Participants
66 adult female Sprague-Dawley rats
Evidence Level
Not specified

Key Findings

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    Application of LPS induced a gradient of inflammation throughout the motor cortex.
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    LPS promoted increased expression of c-Jun and SCG10 for up to 2 weeks, and GAP-43 upregulation for 3 days by many corticospinal neurons.
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    LPS did not promote sprouting of anterogradely labelled corticospinal axons, which did not grow into or beyond a cervical lesion site.

Research Summary

The study investigated the effects of LPS-induced inflammation on the expression of growth-associated genes in corticospinal neurons and the potential for axonal regeneration after spinal cord injury. LPS application induced inflammation in the motor cortex and upregulated growth-associated genes (c-Jun, SCG10, GAP-43) in corticospinal neurons, but had limited effects on ATF3 expression in neurons. Despite increased expression of growth-associated genes, LPS-induced inflammation was insufficient to promote regeneration of the corticospinal tract or sprouting of axons beyond a lesion site.

Practical Implications

Limited Regenerative Potential

Inflammation alone may not be sufficient to induce significant regeneration of corticospinal tract axons after injury.

Growth-Associated Gene Upregulation

Inflammation can upregulate growth-associated genes in corticospinal neurons, suggesting a potential pathway for therapeutic intervention.

Combination Therapies

Future research should explore combining inflammation with other regenerative strategies to enhance axon regeneration.

Study Limitations

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