Spinal Cord Injury, Dendritic Spines and Rac 1
Posted by brain - research neuroscience groupSpinal cord injury (SCI) could determine dendritic spines remodeling and can contribute to neuronal hyperexcitability and neuropathic pain through synaptic changes. Synaptic plasticity induced by SCI may appear in the spinal cord dorsal horn and may contribute to pain maintenance [1,2]. SCI increases Rac1 mRNA expression, which remains elevated for up to 3 months [3]. A role of Rac1, in neuropathic pain after SCI is not studied enough. Rac1 can modulate dendritic spine morphology and function [4, 5]. Andrew M. Tan et al (2008) applied the Rac1-specific inhibitor NSC23766 in order to study the effect of synaptic remodeling in neuropathic pain after SCI. Rac1-specific inhibitor NSC23766 blocks guanine exchange factors (GEFs), Trio and Tiam1. Inhibition of the Rac1 signaling cascade ameliorated the development of abnormal spine morphologies, reduced neuronal excitability, and normalized nociceptive thresholds. [6] PSD-95 expression is a marker of sites of synapse plasticity. Expression of PSD-95 is increased significantly in injured spinal cord tissue compared with uninjured controls [6]. NSC23766 treatment reduces PSD-95 levels below that of uninjured levels . Cortactin levels did not significantly change after NSC23766 treatment compared with intact animals. Dendritic spine density increases after SCI. In SCI plus veh animals (0.9% saline), the density of spines significantly shift toward the cell body compared with the spine density distribution in intact animals. An increase in spine density and redistribution of spine location relative to the cell body, and increases in spine length and head diameter after SCI occurs after SCI in dorsal horn neurons.
1 .Woolf CJ, Shortland P, Coggeshall RE (1992) Peripheral nerve injury triggers central sprouting of myelinated a fferents. Nature 355:75–78.
2. Kim BG, Dai HN, McAtee M, Vicini S, Bregman BS (2006) Remodeling of synaptic structures in the motor cortex following spinal cord injury. Exp Neurol 198:401– 415.
3. Erschbamer MK, Hofstetter CP, Olson L (2005) RhoA, RhoB, RhoC, Rac1, Cdc42, and Tc10 mRNA levels in spinal cord, sensory ganglia, and corticospinal tract neurons and long lasting speci fic changes following spinal cord injury. J Comp Neurol 484:224 –233.
4. Nakayama AY, Harms MB, Luo L (2000) Small GTPases Rac
and Rho in the maintenance of dendritic spines and branches in hippocampal pyramidal neurons. J Neurosci 20:5329–5338.
5. Wiens KM, Lin H, Liao D (2005) Rac1 induces the clustering of AMPA receptors during spinogenesis. J Neurosci 25:10627–10636.
6. Andrew M. Tan, Severine Stamboulian, Yu-Wen Chang, Peng Zhao, Avis B. Hains,2 Stephen G. Waxman, and Bryan C. Hains, Neuropathic Pain Memory Is Maintained by Rac1-Regulated Dendritic Spine Remodeling after Spinal Cord Injury, The Journal of Neuroscience, 28(49):13173–13183 13173
For more about the relation between
Spinal cord injury and Rac1 ,
Dendritic Spines and PSD ,
Rho family of GTPases,
Actin Regulatory Pathways,
Dorsal Horn Neuronal Network and
Medication in SCI see the flash presentation bellow.
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