Spinal cord injury and its underlying mechanism in rats with temporal lobe epilepsy

Abstract

Numerous cases of spinal cord injury following seizure have been previously reported. However, whether spinal cord injury is a common occurrence after seizures and its underlying mechanisms remain unclear. The present study generated a Sprague-Dawley rat model of temporal lobe epilepsy (TLE), and Nissl staining and transmission electron microscopy were used to detect tissue damage. In addition, Evans blue staining was used to detect damage to the blood-brain barrier (BBB) and albumin extravasation. In addition, double-staining was used to detect the association between neurons and extravasated albumin. Furthermore, neuronal degeneration was assessed using Fluoro-Jade C staining, while fluorescence staining and western blotting were used to detect apoptosis and inflammation. In the present study, spinal cord injury was only observed in rats with grade IV-V seizures, whereas Nissl staining showed structural damage and decreased neuronal cell numbers in the brain and the spinal cord. The present study identified BBB damage and albumin extravasation in rats of the TLE groups. Double-staining for albumin and neurons showed a significant match of neurons positive for albumin. Fluoro-Jade C staining indicated neuronal degeneration in the brain, but not the spinal cord in the TLE rats. High levels of caspase-3 were also detected in the injured spinal cord. A small number of albumin + neurons in the spinal cord presented caspase-3 + signals in rats of the TLE groups. The expression levels of intercellular adhesion molecule 1, CD11b and inflammatory factors such as tumor necrosis factor-α and interleukin-6 were significantly elevated in the injured spinal cord. The present results suggested that spinal cord injury occurred in rats as a result of severe seizure attacks, and that BBB damage, albumin extravasation, inflammation and apoptosis contributed to the pathological changes observed during spinal cord injury.

Pannexin-1 Contributes to the Apoptosis of Spinal Neurocytes in Spinal Cord Injury

“…Apoptosis of neurocytes was found around the damaged area in the spinal cord of patients who died of SCI in 3 h to 2 months, with degenerative changes occurred in adjacent segments ( Emery et al, 1998 ). Besides, studies have confirmed that neurocytes necrosis was dominant in the early stage of SCI in rats, and the apoptosis of neurocytes began in 6 h after injury, which could last for 2 weeks or even longer ( Liu et al, 2020 ). Panx1 was correlated with the inflammatory response ( Pelegrin and Surprenant, 2006 ; Orellana et al, 2013 ), Pyroptosis ( Kayagaki et al, 2011 , 2013 ; Hagar et al, 2013 ; de Gassart and Martinon, 2015 ; Yang et al, 2015 ), and autophagy ( Ayna et al, 2012 ; Martins et al, 2014 ) after nervous system injury, which promoted apoptosis in the cells.…”

Quantitative iTRAQ proteomics reveal the proteome profiles of bone marrow mesenchymal stem cells after cocultures with Schwann cells in vitro

“…Among the corresponding changes, ICAM1 was upregulated. ICAM1, which is a single-chain cell surface glycoprotein, is a molecule that has significant roles in the inflammatory response and in the recruitment of leukocytes to sites of inflammation ( 30 , 31 ). ICAM1 promotes adhesion at inflammatory sites and regulates the immune response, which is very beneficial in acute SCI.…”

“…SCs may promote BMSC differentiation into neuron-like cells and co-grafting these two types of cells can improve functional recovery after SCI via the PI3K-Akt signaling pathway. As mentioned above, “CAMs” and “leukocyte transendothelial migration” play crucial roles in regulating adhesion at inflammatory sites and in the immune response ( 30 , 31 ). It has been reported that PPAR activation can induce anti-inflammatory and antioxidant effects, provide vascular protection, and inhibit apoptosis in the nervous system; thus, PPAR may be a novel pharmacological target in neuroprotection ( 50 - 52 ).…”

Protocol paper: kainic acid excitotoxicity-induced spinal cord injury paraplegia in Sprague–Dawley rats

“…The brain and spinal cord share a common origin, which is supported by the co-expression of specific neurotransmitters in both locations. Therefore, SCI and the abnormal discharge of brain neurons producing seizure might be closely related [14]. However, KA follows towards the lower parts and will cause rapid stiffness of the lower limbs and tail, producing paraplegia (paralysis of the lower extremities).…”