Abstract
“Neuroplasticity” is often evoked to explain adaptation and compensation after acute lesions of the Central Nervous System (CNS). In this study, we investigated the modification of 80 genes involved in synaptic plasticity at different times (24 h, 8 and 45 days) from the traumatic spinal cord injury (SCI), adopting a bioinformatic analysis. mRNA expression levels were analyzed in the motor cortex, basal ganglia, cerebellum and in the spinal segments rostral and caudal to the lesion. The main results are: (i) a different gene expression regulation is observed in the Spinal Cord (SC) segments rostral and caudal to the lesion; (ii) long lasting changes in the SC includes the extracellular matrix (ECM) enzymes Timp1, transcription regulators (Egr, Nr4a1), second messenger associated proteins (Gna1, Ywhaq); (iii) long-lasting changes in the Motor Cortex includes transcription regulators (Cebpd), neurotransmitters/neuromodulators and receptors (Cnr1, Gria1, Nos1), growth factors and related receptors (Igf1, Ntf3, Ntrk2), second messenger associated proteins (Mapk1); long lasting changes in Basal Ganglia and Cerebellum include ECM protein (Reln), growth factors (Ngf, Bdnf), transcription regulators (Egr, Cebpd), neurotransmitter receptors (Grin2c). These data suggest the molecular mapping as a useful tool to investigate the brain and SC reorganization after SCI.
Highlights
An acute lesion of the Spinal Cord (SC) is followed by an ensemble of reactive phenomena, embracing the molecular, structural, electrophysiological and functional levels, which involve the lesion site, but all the Central Nervous System (CNS) areas anatomically related and even unrelated to the lesion
In attempt to fill this gap and highlight the molecular substrate of neuroplasticity in spinal cord injury (SCI), in this study we investigated changes in the expression level of genes associated with synaptic plasticity at 24 h, 8 and 45 days after contusive SCI in rats Motor Cortex (CTX-M), Basal Ganglia (BG), Cerebellum (CB) and un-injured SC, rostral and caudal to the lesion level
When considering the cervical SC, that is relatively far from the lesion site, three genes resulted upregulated at 1 days post lesion (DPL) (Cebpd, Cnr1 and Timp1), being Timp1 still overexpressed at 8, but not at 45 DPL
Summary
An acute lesion of the Spinal Cord (SC) is followed by an ensemble of reactive phenomena, embracing the molecular, structural, electrophysiological and functional levels, which involve the lesion site, but all the Central Nervous System (CNS) areas anatomically related and even unrelated to the lesion. Spinal Cord Injury (SCI) in several task-evoked functional magnetic resonance imaging (fMRI) studies [5], and neuroplasticity is currently a focus for rehabilitation approaches [6]. Even though neuroplasticity is regarded as the biological substrate of rehabilitative motor training, and eliciting it represent one of the most widely used approaches to promote moderate recovery following injuries of the CNS, few preclinical data useful for translational purposes are available to support and provide experimental evidence on undergoing molecular and structural events [8]
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