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15 June 2017, Volume 12 Issue 6 Previous Issue    Next Issue

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The crossed phrenic phenomenon Michael George Zaki Ghali 2017, 12 (6):  845-864.  doi: 10.4103/1673-5374.208539 Abstract ( 402 )   PDF (1160KB) ( 612 )   Save The cervical spine is the most common site of traumatic vertebral column injuries. Respiratory insufficiency constitutes a significant proportion of the morbidity burden and is the most common cause of mortality in these patients. In seeking to enhance our capacity to treat specifically the respiratory dysfunction following spinal cord injury, investigators have studied the “crossed phrenic phenomenon”, wherein contraction of a hemidiaphragm paralyzed by a complete hemisection of the ipsilateral cervical spinal cord above the phrenic nucleus can be induced by respiratory stressors and recovers spontaneously over time. Strengthening of latent contralateral projections to the phrenic nucleus and sprouting of new descending axons have been proposed as mechanisms contributing to the observed recovery. We have recently demonstrated recovery of spontaneous crossed phrenic activity occurring over minutes to hours in C1-hemisected unanesthetized decerebrate rats. The specific neurochemical and molecular pathways underlying crossed phrenic activity following injury require further clarification. A thorough understanding of these is necessary in order to develop targeted therapies for respiratory neurorehabilitation following spinal trauma. Animal studies provide preliminary evidence for the utility of neuropharmacological manipulation of serotonergic and adenosinergic pathways, nerve grafts, olfactory ensheathing cells, intraspinal microstimulation and a possible role for dorsal rhizotomy in recovering phrenic activity following spinal cord injury. Related Articles | Metrics

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Immunomodulators and microRNAs as neurorestorative therapy for ischemic stroke Bridget Martinez, Philip V. Peplow 2017, 12 (6):  865-874.  doi: 10.4103/1673-5374.208540 Abstract ( 196 )   PDF (349KB) ( 728 )   Save Most of all strokes are ischemic due to occlusion of a vessel, and comprise two main types, thrombotic and embolic. Inflammation and immune response play an important role in the outcome of ischemic stroke. Pharmaceutical and cell-based therapies with immunomodulatory properties could be of benefit in treating ischemic stroke. Possible changes in microRNAs brought about by immunomodulatory treatments may be important. The pharmaceutical studies described in this review have identified several differentially regulated miRNAs associated with disregulation of mRNA targets or the upregulation of several neuroprotective genes, thereby highlighting the potential neuroprotective roles of specific miRNAs such as miR-762, -1892, -200a, -145. MiR-124, -711, -145 are the strongly associated miRNAs predicted to mediate anti-inflammatory pathways and microglia/macrophage M2-like activation phenotype. The cell-based therapy studies reviewed have mainly utilized mesenchymal stem cells or human umbilical cord blood cells and shown to improve functional and neurological outcomes in stroke animals. MiR-145 and miR-133b were implicated in nerve cell remodeling and functional recovery after stroke. Human umbilical cord blood cells decreased proinflammatory factors and promoted M2 macrophage polarization in stroke diabetic animals. Related Articles | Metrics

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Curcuma longa L. extract improves the cortical neural connectivity during the aging process Gonzalo Flores 2017, 12 (6):  875-880.  doi: 10.4103/1673-5374.208542 Abstract ( 240 )   PDF (291KB) ( 616 )   Save Turmeric or Curcuma is a natural product that has anti-inflammatory, antioxidant and anti-apoptotic pharmacological properties. It can be used in the control of the aging process that involves oxidative stress, inflammation, and apoptosis. Aging is a physiological process that affects higher cortical and cognitive functions with a reduction in learning and memory, limited judgment and deficits in emotional control and social behavior. Moreover, aging is a major risk factor for the appearance of several disorders such as cerebrovascular disease, diabetes mellitus, and hypertension. At the brain level, the aging process alters the synaptic intercommunication by a reduction in the dendritic arbor as well as the number of the dendritic spine in the pyramidal neurons of the prefrontal cortex, hippocampus and basolateral amygdala, consequently reducing the size of these regions. The present review discusses the synaptic changes caused by the aging process and the neuroprotective role the Curcuma has through its anti-inflammatory, antioxidant and anti-apoptotic actions. Related Articles | Metrics

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Novel aspects of extracellular adenosine dynamics revealed by adenosine sensor cells Kunihiko Yamashiro, Mitsuhiro Morita 2017, 12 (6):  881-885.  doi: 10.4103/1673-5374.208544 Abstract ( 184 )   PDF (326KB) ( 324 )   Save activities, blood flow, and inflammation. However, the mechanisms underlying the dynamics of extracellular adenosine are not fully understood. We have recently developed a novel biosensor, called an adenosine sensor cell, and we have characterized the neuronal and astrocytic pathways for elevating extracellular adenosine. In this review, the physiological implications and therapeutic potential of the pathways revealed by the adenosine sensor cells are discussed. We propose that the multiple pathways regulating extracellular adenosine allow for the diverse functions of this neuromodulator, and their malfunctions cause various neurological and psychiatric disorders. Related Articles | Metrics

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Dual and multi-drug delivery nanoparticles towards neuronal survival and synaptic repair Angelina Angelova, Borislav Angelov 2017, 12 (6):  886-889.  doi: 10.4103/1673-5374.208546 Abstract ( 328 )   PDF (540KB) ( 671 )   Save Among the macromolecular drug targets in neurodegenerative disorders, the neurotrophin brain-derived neurotrophic factor (BDNF) and its high-affinity tropomyosin-related kinase receptor (TrkB) present strong interest for nanomedicine development aiming at neuronal and synaptic repair. Currently, BDNF is regarded as the neurotrophic factor of highest therapeutic significance. However, BDNF has delivery problems as a protein drug. The enhanced activation of the transcription factor CREB (cAMP response element-binding protein) has been evidenced to increase the BDNF gene expression and hence the production of endogenous BDNF. We assume that BDNF delivery by nanocarriers and mitochondrial protection may provide high potential for therapeutic amelioration of the neuroregenerative strategies. Beneficial therapeutic outcomes may be expected for synergistic dual or multi-drug action aiming at (i) neurotrophic protein regulation in the central and peripheral nervous systems, and (ii) diminishment of the production of reactive oxygen species (ROS) and the oxidative damage in mitochondria. Our research strategy is based on a nanoarchitectonics approach for the design of nanomedicine assemblies by hierarchical self-assembly. We explore nanoarchitectonics concepts in soft-matter nanotechnology towards preparation of biodegradable self-assembled lipid nanostructures for safe neuro-therapeutic applications of multi-target nanomedicines. Related Articles | Metrics

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Neurological consequences of systemic inflammation in the premature neonate Aparna Patra, Hong Huang, John A. Bauer, Peter J. Giannone 2017, 12 (6):  890-896.  doi: 10.4103/1673-5374.208547 Abstract ( 271 )   PDF (293KB) ( 378 )   Save Despite substantial progress in neonatal care over the past two decades leading to improved survival of extremely premature infants, extreme prematurity continues to be associated with long term neurodevelopmental impairments. Cerebral white matter injury is the predominant form of insult in preterm brain leading to adverse neurological consequences. Such brain injury pattern and unfavorable neurologic sequelae is commonly encountered in premature infants exposed to systemic inflammatory states such as clinical or culture proven sepsis with or without evidence of meningitis, prolonged mechanical ventilation, bronchopulmonary dysplasia, necrotizing enterocolitis and chorioamnionitis. Underlying mechanisms may include cytokine mediated processes without direct entry of pathogens into the brain, developmental differences in immune response and complex neurovascular barrier system that play a critical role in regulating the cerebral response to various systemic inflammatory insults in premature infants. Understanding of these pathologic mechanisms and clinical correlates of such injury based on serum biomarkers or brain imaging findings on magnetic resonance imaging will pave way for future research and translational therapeutic opportunities for the developing brain. Related Articles | Metrics

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On the role of endogenous neurotoxins and neuroprotection in Parkinson’s disease Juan Segura-Aguilar 2017, 12 (6):  897-901.  doi: 10.4103/1673-5374.208560 Abstract ( 249 )   PDF (746KB) ( 842 )   Save For 50 years ago was introduced L-3,4-dihydroxyphenylalanine (L-dopa) in Parkinson’s disease treatment and during this significant advances has been done but what trigger the degeneration of the nigrostriatal system remain unknown. There is a general agreement in the scientific community that mitochondrial dysfunction, protein degradation dysfunction, alpha-synuclein aggregation to neurotoxic oligomers, neuroinflammation, oxidative and endoplasmic reticulum stress are involved in the loss of dopaminergic neurons containing neuromelanin in Parkinson’s disease. The question is what triggers these mechanisms. The age of normal onset in idiopathic Parkinson’s disease suggests that environmental factors such as metals, pollutants or genetic mutations cannot be involved because these factors are related to early onset of Parkinsonism. Therefore, we have to search for endogenous neurotoxins and neuroprotection in order to understand what trigger the loss of dopaminergic neurons. One important feature of Parkinson’s disease is the rate of the degenerative process before the motor symptoms are evident and during the disease progression. The extremely slow rate of Parkinson’s disease suggests that the neurotoxins and the neuroprotection have to be related to dopamine metabolism. Possible candidates for endogenous neurotoxins are alpha-synuclein neurotoxic oligomers, 4-dihydroxyphenylacetaldehyde and ortho-quinones formed during dopamine oxidation to neuromelanin. Vesicular monoamine transporter-2, DT-diaphorase and glutathione transferase M2-2 seems to be the most important neuroprotective mechanism to prevent neurotoxic mechanism during dopamine oxidation. Related Articles | Metrics

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The interaction of genetics and environmental toxicants in amyotrophic lateral sclerosis: results from animal models Roger B. Sher 2017, 12 (6):  902-905.  doi: 10.4103/1673-5374.208564 Abstract ( 234 )   PDF (363KB) ( 556 )   Save Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that results in the progressive death of motor neurons, leading to paralysis and eventual death. There is presently no cure for ALS, and only two drugs are available, neither of which provide significant extension of life. The wide variation in onset and progression of the disease, both in sporadic and even in strongly penetrant monogenic familial forms of ALS, indicate that in addition to background genetic variation impacting the disease process, environmental exposures are likely contributors. Epidemiological evidence worldwide implicates exposures to bacterial toxins, heavy metals, pesticides, and trauma as probable environmental factors. Here, we review current advances in gene-environment interactions in ALS animal models. We report our recent discoveries in a zebrafish model of ALS in relation to exposure to the cyanobacterial toxin BMAA, and discuss several results from mouse models that show interactions with exposure to mercury and statin drugs, both leading to acceleration of the disease process. The increasing research into this combinatorial gene-environment process is just starting, but shows early promise to uncover the underlying biochemical pathways that instigate the initial motor neuron defects and lead to their rapidly progressive dysfunction. Related Articles | Metrics

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Interfacing peripheral nerve with macro-sieve electrodes following spinal cord injury Nathan K. Birenbaum, Matthew R. MacEwan, Wilson Z. Ray 2017, 12 (6):  906-909.  doi: 10.4103/1673-5374.208565 Abstract ( 249 )   PDF (422KB) ( 575 )   Save Macro-sieve electrodes were implanted in the sciatic nerve of five adult male Lewis rats following spinal cord injury to assess the ability of the macro-sieve electrode to interface regenerated peripheral nerve fibers post-spinal cord injury. Each spinal cord injury was performed via right lateral hemisection of the cord at the T9–10 site. Five months post-implantation, the ability of the macro-sieve electrode to interface the regenerated nerve was assessed by stimulating through the macro-sieve electrode and recording both electromyography signals and evoked muscle force from distal musculature. Electromyography measurements were recorded from the tibialis anterior and gastrocnemius muscles, while evoked muscle force measurements were recorded from the tibialis anterior, extensor digitorum longus, and gastrocnemius muscles. The macro-sieve electrode and regenerated sciatic nerve were then explanted for histological evaluation. Successful sciatic nerve regeneration across the macro-sieve electrode interface following spinal cord injury was seen in all five animals. Recorded electromyography signals and muscle force recordings obtained through macro-sieve electrode stimulation confirm the ability of the macro-sieve electrode to successfully recruit distal musculature in this injury model. Taken together, these results demonstrate the macro-sieve electrode as a viable interface for peripheral nerve stimulation in the context of spinal cord injury. Related Articles | Metrics

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Repurposing cancer drugs to treat neurological diseases – Src inhibitors as examples Da Zhi Liu 2017, 12 (6):  910-911.  doi: 10.4103/1673-5374.208569 Abstract ( 171 )   PDF (379KB) ( 331 )   Save Related Articles | Metrics

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The use of localized proteomics to identify the drivers of Alzheimer’s disease pathogenesis Eleanor Drummond, Thomas Wisniewski 2017, 12 (6):  912-913.  doi: 10.4103/1673-5374.208570 Abstract ( 144 )   PDF (130KB) ( 399 )   Save Related Articles | Metrics

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Heparan sulfate proteoglycans and heparanases in Alzheimer’s disease: current outlook and potential therapeutic targets Laura Lorente-Gea, Beatriz García, Carla Martín, Luis M. Quirós, Iván Fernández-Vega 2017, 12 (6):  914-915.  doi: 10.4103/1673-5374.208571 Abstract ( 300 )   PDF (243KB) ( 372 )   Save Related Articles | Metrics

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Galantamine protects against beta amyloid peptide-induced DNA damage in a model for Alzheimer’s disease Willian O. Castillo, Andres Felipe Aristizabal-Pachon 2017, 12 (6):  916-917.  doi: 10.4103/1673-5374.208572 Abstract ( 274 )   PDF (297KB) ( 512 )   Save Related Articles | Metrics

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Neuroprotective effects of ischemic preconditioning on hippocampal CA1 pyramidal neurons through maintaining calbindin D28k immunoreactivity following subsequent transient cerebral ischemia In Hye Kim, Yong Hwan Jeon, Tae-Kyeong Lee, Jeong Hwi Cho, Jae-Chul Lee, Joon Ha Park, Ji Hyeon Ahn, Bich-Na Shin, Yang Hee Kim, Seongkweon Hong, Bing Chun Yan, Moo-Ho Won, Yun Lyul Lee 2017, 12 (6):  918-924.  doi: 10.4103/1673-5374.208573 Abstract ( 265 )   PDF (2586KB) ( 703 )   Save Ischemic preconditioning elicited by a non-fatal brief occlusion of blood flow has been applied for an experimental therapeutic strategy against a subsequent fatal ischemic insult. In this study, we investigated the neuroprotective effects of ischemic preconditioning (2-minute transient cerebral ischemia) on calbindin D28k immunoreactivity in the gerbil hippocampal CA1 area following a subsequent fatal transient ischemic insult (5-minute transient cerebral ischemia). A large number of pyramidal neurons in the hippocampal CA1 area died 4 days after 5-minute transient cerebral ischemia. Ischemic preconditioning reduced the death of pyramidal neurons in the hippocampal CA1 area. Calbindin D28k immunoreactivity was greatly attenuated at 2 days after 5-minute transient cerebral ischemia and it was hardly detected at 5 days post-ischemia. Ischemic preconditioning maintained calbindin D28k immunoreactivity after transient cerebral ischemia. These findings suggest that ischemic preconditioning can attenuate transient cerebral ischemia-caused damage to the pyramidal neurons in the hippocampal CA1 area through maintaining calbindin D28k immunoreactivity. Related Articles | Metrics

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Electroacupuncture regulates the stress-injury-repair chain of events after cerebral ischemia/reperfusion injury Peng Shi, Lin-lin Sun, Yi-shuo Lee, Ya Tu 2017, 12 (6):  925-930.  doi: 10.4103/1673-5374.208574 Abstract ( 203 )   PDF (900KB) ( 632 )   Save Inflammation after stroke is the main cause of cerebral ischemia/reperfusion injury. Cascading events after injury can lead to cell death. Heat shock protein 70 and other endogenous injury-signaling molecules are released by damaged cells, which can lead to systemic stress reactions. Protecting the brain through repair begins with the stress-injury-repair signaling chain. This study aimed to verify whether acupuncture acts through this chain to facilitate effective treatment of ischemic stroke. Rat models of cerebral ischemia/reperfusion injury were established by Zea Longa’s method, and injury sites were identified by assessing neurological function, 2,3,5-triphenyltetrazolium chloride staining, and hematoxylin-eosin staining. Electroacupuncture at acupoints Baihui (DU20) and Zusanli (ST36) was performed in the model rats with dilatational waves, delivered for 20 minutes a day at 2–100 Hz and an amplitude of 2 mA. We analyzed the blood serum from the rats and found that inflammatory cytokines affected the levels of adrenotrophin and heat shock protein 70, each of which followed a similar bimodal curve. Specifically, electroacupuncture lowered the peak levels of adrenocorticotrophic hormone and heat shock protein 70. Thus, electroacupuncture was able to inhibit excessive stress, reduce inflammation, and promote the repair of neurons, which facilitated healing of ischemic stroke. Related Articles | Metrics

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Metabolite changes in the ipsilateral and contralateral cerebral hemispheres in rats with middle cerebral artery occlusion Lei Ruan, Yan Wang, Shu-chao Chen, Tian Zhao, Qun Huang,Z i-long Hu, Neng-zhi Xia, Jin-jin Liu, Wei-jian Chen, Yong Zhang, Jing-liang Cheng, Hong-chang Gao, Yun-jun Yang, Hou-zhang Sun 2017, 12 (6):  931-937.  doi: 10.4103/1673-5374.208575 Abstract ( 233 )   PDF (586KB) ( 570 )   Save Cerebral ischemia not only causes pathological changes in the ischemic areas but also induces a series of secondary changes in more distal brain regions (such as the contralateral cerebral hemisphere). The impact of supratentorial lesions, which are the most common type of lesion, on the contralateral cerebellum has been studied in patients by positron emission tomography, single photon emission computed tomography, magnetic resonance imaging and diffusion tensor imaging. In the present study, we investigated metabolite changes in the contralateral cerebral hemisphere after supratentorial unilateral ischemia using nuclear magnetic resonance spectroscopy-based metabonomics. The permanent middle cerebral artery occlusion model of ischemic stroke was established in rats. Rats were randomly divided into the middle cerebral artery occlusion 1-, 3-, 9- and 24-hour groups and the sham group. 1H nuclear magnetic resonance spectroscopy was used to detect metabolites in the left and right cerebral hemispheres. Compared with the sham group, the concentrations of lactate, alanine, γ-aminobutyric acid, choline and glycine in the ischemic cerebral hemisphere were increased in the acute stage, while the concentrations of N-acetyl aspartate, creatinine, glutamate and aspartate were decreased. This demonstrates that there is an upregulation of anaerobic glycolysis (shown by the increase in lactate), a perturbation of choline metabolism (suggested by the increase in choline), neuronal cell damage (shown by the decrease in N-acetyl aspartate) and neurotransmitter imbalance (evidenced by the increase in γ-aminobutyric acid and glycine and by the decrease in glutamate and aspartate) in the acute stage of cerebral ischemia. In the contralateral hemisphere, the concentrations of lactate, alanine, glycine, choline and aspartate were increased, while the concentrations of γ-aminobutyric acid, glutamate and creatinine were decreased. This suggests that there is a difference in the metabolite changes induced by ischemic injury in the contralateral and ipsilateral cerebral hemispheres. Our findings demonstrate the presence of characteristic changes in metabolites in the contralateral hemisphere and suggest that they are most likely caused by metabolic changes in the ischemic hemisphere. Related Articles | Metrics

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High-frequency and brief-pulse stimulation pulses terminate cortical electrical stimulation-induced afterdischarges Zhi-wei Ren, Yong-jie Li, Tao Yu, Duan-yu Ni, Guo-jun Zhang, Wei Du, Yuan-yuan Piao, Xiao-xia Zhou 2017, 12 (6):  938-944.  doi: 10.4103/1673-5374.208576 Abstract ( 295 )   PDF (932KB) ( 587 )   Save Brief-pulse stimulation at 50 Hz has been shown to terminate afterdischarges observed in epilepsy patients. However, the optimal pulse stimulation parameters for terminating cortical electrical stimulation-induced afterdischarges remain unclear. In the present study, we examined the effects of different brief-pulse stimulation frequencies (5, 50 and 100 Hz) on cortical electrical stimulation-induced afterdischarges in 10 patients with refractory epilepsy. Results demonstrated that brief-pulse stimulation could terminate cortical electrical stimulation-induced afterdischarges in refractory epilepsy patients. In conclusion, (1) a brief-pulse stimulation was more effective when the afterdischarge did not extend to the surrounding brain area. (2) A higher brief-pulse stimulation frequency (especially 100 Hz) was more likely to terminate an afterdischarge. (3) A low current intensity of brief-pulse stimulation was more likely to terminate an afterdischarge. Related Articles | Metrics

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Monosialoganglioside 1 may alleviate neurotoxicity induced by propofol combined with remifentanil in neural stem cells Jiang Lu, Xue-qin Yao, Xin Luo, Yu Wang, Sookja Kim Chung, He-xin Tang, Chi Wai Cheung, Xian-yu Wang, Chen Meng, Qing Li 2017, 12 (6):  945-952.  doi: 10.4103/1673-5374.208589 Abstract ( 280 )   PDF (1303KB) ( 585 )   Save Monosialoganglioside 1 (GM1) is the main ganglioside subtype and has neuroprotective properties in the central nervous system. In this study, we aimed to determine whether GM1 alleviates neurotoxicity induced by moderate and high concentrations of propofol combined with remifentanil in the immature central nervous system. Hippocampal neural stem cells were isolated from newborn Sprague-Dawley rats and treated with remifentanil (5, 10, 20 ng/mL) and propofol (1.0, 2.5, 5.0 μg/mL), and/or GM1 (12.5, 25, 50 μg/mL). GM1 reversed combined propofol and remifentanil-induced decreases in the percentage of 5-bromodeoxyuridine(+) cells and also reversed the increase in apoptotic cell percentage during neural stem cell proliferation and differentiation. However, GM1 with combined propofol and remifentanil did not affect β-tubulin(+) or glial fibrillary acidic protein(+) cell percentage during neural stem cell differentiation. In conclusion, we show that GM1 alleviates the damaging effects of propofol combined with remifentanil at moderate and high exposure concentrations in neural stem cells in vitro, and exerts protective effects on the immature central nervous system. Related Articles | Metrics

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Neuroprotective effects of ganoderma lucidum polysaccharides against oxidative stress-induced neuronal apoptosis Xin-zhi Sun, Ying Liao, Wei Li, Li-mei Guo 2017, 12 (6):  953-958.  doi: 10.4103/1673-5374.208590 Abstract ( 315 )   PDF (1045KB) ( 758 )   Save Ganoderma lucidum polysaccharides have protective effects against apoptosis in neurons exposed to ischemia/reperfusion injury, but the mechanisms are unclear. The goal of this study was to investigate the underlying mechanisms of the effects of ganoderma lucidum polysaccharides against oxidative stress-induced neuronal apoptosis. Hydrogen peroxide (H2O2) was used to induce apoptosis in cultured cerebellar granule cells. In these cells, ganoderma lucidum polysaccharides remarkably suppressed H2O2-induced apoptosis, decreased expression of caspase-3, Bax and Bim and increased that of Bcl-2. These findings suggested that ganoderma lucidum polysaccharides regulate expression of apoptosis-associated proteins, inhibit oxidative stress-induced neuronal apoptosis and, therefore, have significant neuroprotective effects. Related Articles | Metrics

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Mechanisms underlying the promotion of functional recovery by deferoxamine after spinal cord injury in rats Jian Hao, Bo Li, Hui-quan Duan, Chen-xi Zhao, Yan Zhang, Chao Sun, Bin Pan, Chang Liu, Xiao-hong Kong, Xue Yao, Shi-qing Feng 2017, 12 (6):  959-968.  doi: 10.4103/1673-5374.208591 Abstract ( 349 )   PDF (2835KB) ( 748 )   Save Deferoxamine, a clinically safe drug used for treating iron overload, also repairs spinal cord injury although the mechanism for this action remains unknown. Here, we determined whether deferoxamine was therapeutic in a rat model of spinal cord injury and explored potential mechanisms for this effect. Spinal cord injury was induced by impacting the spinal cord at the thoracic T10 vertebra level. One group of injured rats received deferoxamine, a second injured group received saline, and a third group was sham operated. Both 2 days and 2 weeks after spinal cord injury, total iron ion levels and protein expression levels of the proinflammatory cytokines tumor necrosis factor-α and interleukin-1β and the pro-apoptotic protein caspase-3 in the spinal cords of the injured deferoxamine-treated rats were significantly lower than those in the injured saline-treated group. The percentage of the area positive for glial fibrillary acidic protein immunoreactivity and the number of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells were also significantly decreased both 2 days and 2 weeks post injury, while the number of NeuN-positive cells and the percentage of the area positive for the oligodendrocyte marker CNPase were increased in the injured deferoxamine-treated rats. At 14–56 days post injury, hind limb motor function in the deferoxamine-treated rats was superior to that in the saline-treated rats. These results suggest that deferoxamine decreases total iron ion, tumor necrosis factor-α, interleukin-1β, and caspase-3 expression levels after spinal cord injury and inhibits apoptosis and glial scar formation to promote motor function recovery. Related Articles | Metrics

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Synaptosomal-associated protein 25 may be an intervention target for improving sensory and locomotor functions after spinal cord contusion Zhan-qiong Zhong, Yang Xiang, Xi Hu, You-cui Wang, Xi Zeng, Xiao-meng Wang, Qing-jie Xia, Ting-hua Wang, Xiao Zhang 2017, 12 (6):  969-976.  doi: 10.4103/1673-5374.208592 Abstract ( 296 )   PDF (2363KB) ( 625 )   Save Synaptosomal-associated protein 25 kDa (SNAP-25) is localized on the synapse and participates in exocytosis and neurotransmitter release. Decreased expression of SNAP-25 is associated with Alzheimer’s disease and attention deficit/hyperactivity disorder. However, the expression of SNAP-25 in spinal cord contusion injury is still unclear. We hypothesized that SNAP-25 is associated with sensory and locomotor functions after spinal cord injury. We established rat models of spinal cord contusion injury to detect gene changes with a gene array. A decreased level of SNAP-25 was detected by quantitative real time-polymerase chain reaction and western blot assay at 1, 3, 7, 14 and 28 days post injury. SNAP-25 was localized in the cytoplasm of neurons of the anterior and posterior horns, which are involved in locomotor and sensory functions. Our data suggest that reduced levels of SNAP-25 are associated with sensory and locomotor functions in rats with spinal cord contusion injury. Related Articles | Metrics

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Effects of pulsed radiofrequency on spasticity in patients with spinal cord injury: a report of two cases Min Cheol Chang, Yun Woo Cho 2017, 12 (6):  977-980.  doi: 10.4103/1673-5374.208593 Abstract ( 395 )   PDF (295KB) ( 420 )   Save Spasticity following spinal cord injury (SCI) results in functional deterioration and reduced quality of life. Herein, we report two SCI patients who presented with good response to pulsed radiofrequency (PRF) for the management of spasticity in the lower extremities. Patient 1 (a 47-year-old man) had complete thoracic cord injury and showed a phasic spasticity on the extensor of both knees (3–4 beats clonus per every 30 seconds) and tonic spasticity (Modified Ashworth Scale: 3) on both hip adductors. Patient 2 (a 64-year-old man) had incomplete cervical cord injury and showed a right ankle clonus (approximately 20 beats) when he walked. After the application of PRF to both L2 and L3 dorsal root ganglion (DRG) (patient 1) and right S1 DRG (patient 2) with 5 Hz and 5 ms pulsed width for 360 seconds at 45V under the C-arm guide, all spasticity disappeared or was reduced. Moreover, the effects of PRF were sustained for approximately 6 months with no side effects. We believe that PRF treatment can be useful for patients with spasticity after SCI. Related Articles | Metrics

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Mild closed head traumatic brain injury-induced changes in monoamine neurotransmitters in the trigeminal subnuclei of a rat model: mechanisms underlying orofacial allodynias and headache Golam Mustafa, Jiamei Hou, Rachel Nelson, Shigeharu Tsuda, Mansura Jahan, Naweed S. Mohammad, Joseph V. Watts, Floyd J. Thompson, Prodip Bose 2017, 12 (6):  981-986.  doi: 10.4103/1673-5374.208594 Abstract ( 281 )   PDF (1598KB) ( 606 )   Save Our recent findings have demonstrated that rodent models of closed head traumatic brain injury exhibit comprehensive evidence of progressive and enduring orofacial allodynias, a hypersensitive pain response induced by non-painful stimulation. These allodynias, tested using thermal hyperalgesia, correlated with changes in several known pain signaling receptors and molecules along the trigeminal pain pathway, especially in the trigeminal nucleus caudalis. This study focused to extend our previous work to investigate the changes in monoamine neurotransmitter immunoreactivity changes in spinal trigeminal nucleus oralis, pars interpolaris and nucleus tractus solitaries following mild to moderate closed head traumatic brain injury, which are related to tactile allodynia, touch-pressure sensitivity, and visceral pain. Our results exhibited significant alterations in the excitatory monoamine, serotonin, in spinal trigeminal nucleus oralis and pars interpolaris which usually modulate tactile and mechanical sensitivity in addition to the thermal sensitivity. Moreover, we also detected a robust alteration in the expression of serotonin, and inhibitory molecule norepinephrine in the nucleus tractus solitaries, which might indicate the possibility of an alteration in visceral pain, and existence of other morbidities related to solitary nucleus dysfunction in this rodent model of mild to moderate closed head traumatic brain injury. Collectively, widespread changes in monoamine neurotransmitter may be related to orofacial allodynhias and headache after traumatic brain injury. Related Articles | Metrics

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Brain injury in combination with tacrolimus promotes the regeneration of injured peripheral nerves Xin-ze He, Jian-jun Ma, Hao-qi Wang, Tie-min Hu, Bo Sun, Yun-feng Gao, Shi-bo Liu, Wei Wang, Pei Wang 2017, 12 (6):  987-994.  doi: 10.4103/1673-5374.208595 Abstract ( 304 )   PDF (3183KB) ( 639 )   Save Both brain injury and tacrolimus have been reported to promote the regeneration of injured peripheral nerves. In this study, before transection of rat sciatic nerve, moderate brain contusion was (or was not) induced. After sciatic nerve injury, tacrolimus, an immunosuppressant, was (or was not) intraperitoneally administered. At 4, 8 and 12 weeks after surgery, Masson’s trichrome, hematoxylin-eosin, and toluidine blue staining results revealed that brain injury or tacrolimus alone or their combination alleviated gastrocnemius muscle atrophy and sciatic nerve fiber impairment on the experimental side, simultaneously improved sciatic nerve function, and increased gastrocnemius muscle wet weight on the experimental side. At 8 and 12 weeks after surgery, brain injury induction and/or tacrolimus treatment increased action potential amplitude in the sciatic nerve trunk. Horseradish peroxidase retrograde tracing revealed that the number of horseradish peroxidase-positive neurons in the anterior horn of the spinal cord was greatly increased. Brain injury in combination with tacrolimus exhibited better effects on repair of injured peripheral nerves than brain injury or tacrolimus alone. This result suggests that brain injury in combination with tacrolimus promotes repair of peripheral nerve injury. Related Articles | Metrics

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Critical signaling pathways during Wallerian degeneration of peripheral nerve Qiong Cheng, Ya-xian Wang, Jun Yu, Sheng Yi 2017, 12 (6):  995-1002.  doi: 10.4103/1673-5374.208596 Abstract ( 367 )   PDF (863KB) ( 1122 )   Save Wallerian degeneration is a critical biological process that occurs in distal nerve stumps after nerve injury. To systematically investigate molecular changes underlying Wallerian degeneration, we used a rat sciatic nerve transection model to examine microarray analysis outcomes and investigate significantly involved Kyoto Enrichment of Genes and Genomes (KEGG) pathways in injured distal nerve stumps at 0, 0.5, 1, 6, 12, and 24 hours, 4 days, 1, 2, 3, and 4 weeks after peripheral nerve injury. Bioinformatic analysis showed that only one KEGG pathway (cytokine-cytokine receptor interaction) was significantly enriched at an early time point (1 hour post-sciatic nerve transection). At later time points, the number of enriched KEGG pathways initially increased and then decreased. Three KEGG pathways were studied in further detail: cytokine-cytokine receptor interaction, neuroactive ligand-receptor interaction, and axon guidance. Moreover, temporal expression patterns of representative differentially expressed genes in these KEGG pathways were validated by real time-polymerase chain reaction. Taken together, the above three signaling pathways are important after sciatic nerve injury, and may increase our understanding of the molecular mechanisms underlying Wallerian degeneration. Related Articles | Metrics

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Polyethylene glycol as a promising synthetic material for repair of spinal cord injury Xian-bin Kong, Qiu-yan Tang, Xu-yi Chen, Yue Tu, Shi-zhong Sun, Zhong-lei Sun 2017, 12 (6):  1003-1008.  doi: 10.4103/1673-5374.208597 Abstract ( 325 )   PDF (228KB) ( 632 )   Save Polyethylene glycol is a synthetic, biodegradable, and water-soluble polyether. Owing to its good biological and material properties, polyethylene glycol shows promise in spinal cord tissue engineering applications. Although studies have examined repairing spinal cord injury with polyethylene glycol, these compelling findings have not been recently reviewed or evaluated as a whole. Thus, we herein review and summarize the findings of studies conducted both within and beyond China that have examined the repair of spinal cord injury using polyethylene glycol. The following summarizes the results of studies using polyethylene glycol alone as well as coupled with polymers or hydrogels: (1) polyethylene glycol as an adjustable biomolecule carrier resists nerve fiber degeneration, reduces the inflammatory response, inhibits vacuole and scar formation, and protects nerve membranes in the acute stage of spinal cord injury. (2) Polyethylene glycol-coupled polymers not only promote angiogenesis but also carry drugs or bioactive molecules to the injury site. Because such polymers cross both the blood-spinal cord and blood-brain barriers, they have been widely used as drug carriers. (3) Polyethylene glycol hydrogels have been used as supporting substrates for the growth of stem cells after injury, inducing cell migration, proliferation, and differentiation. Simultaneously, polyethylene glycol hydrogels isolate or reduce local glial scar invasion, promote and guide axonal regeneration, cross the transplanted area, and re-establish synaptic connections with target tissue, thereby promoting spinal cord repair. On the basis of the reviewed studies, we conclude that polyethylene glycol is a promising synthetic material for use in the repair of spinal cord injury. Related Articles | Metrics