Abstract
BackgroundInflammation around cell bodies of primary sensory neurons and retinal ganglion cells enhances expression of neuronal growth-associated genes and stimulates axonal regeneration. We have asked if inflammation would have similar effects on corticospinal neurons, which normally show little response to spinal cord injury. Lipopolysaccharide (LPS) was applied onto the pial surface of the motor cortex of adult rats with or without concomitant injury of the corticospinal tract at C4. Inflammation around corticospinal tract cell bodies in the motor cortex was assessed by immunohistochemistry for OX42 (a microglia and macrophage marker). Expression of growth-associated genes c-jun, ATF3, SCG10 and GAP-43 was investigated by immunohistochemistry or in situ hybridisation.ResultsApplication of LPS induced a gradient of inflammation through the full depth of the motor cortex and promoted c-Jun and SCG10 expression for up to 2 weeks, and GAP-43 upregulation for 3 days by many corticospinal neurons, but had very limited effects on neuronal ATF3 expression. However, many glial cells in the subcortical white matter upregulated ATF3. LPS did not promote sprouting of anterogradely labelled corticospinal axons, which did not grow into or beyond a cervical lesion site.ConclusionInflammation produced by topical application of LPS promoted increased expression of some growth-associated genes in the cell bodies of corticospinal neurons, but was insufficient to promote regeneration of the corticospinal tract.
Highlights
Inflammation around cell bodies of primary sensory neurons and retinal ganglion cells enhances expression of neuronal growth-associated genes and stimulates axonal regeneration
BMC Neuroscience 2006, 7:8 http://www.biomedcentral.com/1471-2202/7/8. Against this background we have investigated the possibility that LPS-induced inflammation around the cell bodies of corticospinal tract neurons would enhance their expression of growth-associated genes (c-jun, ATF3, SCG10 and GAP-43) and promote regeneration of their axons following spinal cord injury
Assessing LPS-induced inflammation in cortex Coronal sections through the motor cortex to which LPS had been applied were immunostained with OX42, an antibody that recognizes the type 3 complement receptor (CR3) in mononuclear phagocytes, which is upregulated by activated microglia and macrophages [9]
Summary
Inflammation around cell bodies of primary sensory neurons and retinal ganglion cells enhances expression of neuronal growth-associated genes and stimulates axonal regeneration. Against this background we have investigated the possibility that LPS-induced inflammation around the cell bodies of corticospinal tract neurons would enhance their expression of growth-associated genes (c-jun, ATF3, SCG10 and GAP-43) and promote regeneration of their axons following spinal cord injury. It is of particular importance and interest to investigate these questions in relation to corticospinal neurons because their axons constitute the major descending motor pathway, and because they display very poor regenerative responses to injury. Corticospinal neurons do not regenerate axons to any significant extent along peripheral nerve grafts inserted into the spinal cord or brainstem [4,5,6] and display upregulation of growthassociated genes only after intracortical lesion of their axons and not after spinal injury [7,8]
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