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The present study aimed to assess the molecular bases of cortical compensatory mechanisms following spinal cord injury in primates. To accomplish this, comprehensive changes in gene expression were investigated in the bilateral primary motor cortex (M1), dorsal premotor cortex (PMd), and ventral premotor cortex (PMv) after a unilateral lesion of the lateral corticospinal tract (l-CST). At 2 weeks after the lesion, a large number of genes exhibited altered expression levels in the contralesional M1, which is directly linked to the lesioned l-CST. Gene ontology and network analyses indicated that these changes in gene expression are involved in the atrophy and plasticity changes observed in neurons. Orchestrated gene expression changes were present when behavioral recovery was attained 3 months after the lesion, particularly among the bilateral premotor areas, and a large number of these genes are involved in plasticity. Moreover, several genes abundantly expressed in M1 of intact monkeys were upregulated in both the PMd and PMv after the l-CST lesion. These area-specific and time-dependent changes in gene expression may underlie the molecular mechanisms of functional recovery following a lesion of the l-CST.
Pubmed ID: 29355954 RIS Download
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This polyclonal targets Rabbit Glial Fibrillary Acidic Protein (GFAP)
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View all literature mentionsThis polyclonal targets Rabbit Glial Fibrillary Acidic Protein (GFAP)
View all literature mentionsThis monoclonal targets NeuN clone A60 Alexa Fluor 488 conjugated
View all literature mentionsThis polyclonal targets Rabbit Glial Fibrillary Acidic Protein (GFAP)
View all literature mentionsThis monoclonal targets NeuN clone A60 Alexa Fluor 488 conjugated
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