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Spinal plasticity

Katherine Whalley
No abstract text is available yet for this article.
October 20, 2016: Nature Reviews. Neuroscience
Dong-Hee Choi, Jin-Hee Ahn, In-Ae Choi, Ji-Hye Kim, Bo-Ram Kim, Jongmin Lee
Recent evidence indicates that the ephrin receptors and ephrin ligands (Eph/ephrin) expression modulates axonal reorganization and synaptic plasticity in stroke recovery. To investigate the effect of task-specific training (TST) on Eph/ephrin expression in the corticospinal tract (CST) after stroke, we compared Eph/ephrin expression in the peri-infarct cortex, pyramid, and spinal cord of the photothrombotic stroke rats treated with or without TST. The TST treatment showed significantly better recovery in the behavioral tests...
October 19, 2016: BMB Reports
Meagan E Ita, Nathan D Crosby, Ben A Bulka, Beth A Winkelstein
STUDY DESIGN: Immunohistochemistry labeled pre- and post-synaptic structural markers to quantify excitatory and inhibitory synapses in the spinal superficial dorsal horn at 14 days after painful facet joint injury in the rat. OBJECTIVE: The objective of this study was to investigate the relationship between pain and synapse density in the spinal cord after facet injury. SUMMARY OF BACKGROUND DATA: Neck pain is a major contributor to disability and often becomes chronic...
October 17, 2016: Spine
Thomas Broggini, Lisa Schnell, Ali Ghoochani, José María Mateos, Michael Buchfelder, Kurt Wiendieck, Michael K Schäfer, Ilker Y Eyupoglu, Nicolai E Savaskan
The Plasticity Related Gene family covers five, brain-specific, transmembrane proteins (PRG1-5, also termed LPPR1-5) that operate in neuronal plasticity during development, aging and brain trauma. Here we investigated the role of the PRG family on axonal and filopodia outgrowth. Comparative analysis revealed the strongest outgrowth induced by PRG3 (LPPR1). During development, PRG3 is ubiquitously located at the tip of neuronal processes and at the plasma membrane and declines with age. In utero electroporation of PRG3 induced dendritic protrusions and accelerated spine formations in cortical pyramidal neurons...
October 15, 2016: Aging
Yingli Jing, Fan Bai, Hui Chen, Hao Dong
BACKGROUND: Melatonin can be neuroprotective in models of neurological injury, but its effects on blood vessel loss and neurological impairment following spinal cord injury (SCI) are unclear. Our goal herein was to evaluate the possible protective action of melatonin on the above SCI-induced damage in rats. MATERIALS AND METHODS: Sixty-three female Sprague-Dawley rats were randomly divided into three equal groups: sham, SCI and melatonin groups. Melatonin (10 mg/kg) was injected intraperitoneally and further administered twice a day at indicated time after a moderate injury at T10 in melatonin group...
October 13, 2016: Journal of Spinal Cord Medicine
Atif S Khan, Susan K Patrick, Francois D Roy, Monica A Gorassini, Jaynie F Yang
The neural plasticity of spinal reflexes after two contrasting forms of walking training was determined in individuals with chronic, motor-incomplete spinal cord injury (SCI). Endurance Training involved treadmill walking for as long as possible, and Precision Training involved walking precisely over obstacles and onto targets overground. Twenty participants started either Endurance or Precision Training for 2 months and then crossed over after a 2-month rest period to the other form of training for 2 months...
2016: Neural Plasticity
Sandra M Garraway, J Russell Huie
Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic factor family of signaling molecules. Since its discovery over three decades ago, BDNF has been identified as an important regulator of neuronal development, synaptic transmission, and cellular and synaptic plasticity and has been shown to function in the formation and maintenance of certain forms of memory. Neural plasticity that underlies learning and memory in the hippocampus shares distinct characteristics with spinal cord nociceptive plasticity...
2016: Neural Plasticity
Andrea Tedeschi, Sebastian Dupraz, Claudia J Laskowski, Jia Xue, Thomas Ulas, Marc Beyer, Joachim L Schultze, Frank Bradke
Injuries to the adult CNS often result in permanent disabilities because neurons lose the ability to regenerate their axon during development. Here, whole transcriptome sequencing and bioinformatics analysis followed by gain- and loss-of-function experiments identified Cacna2d2, the gene encoding the Alpha2delta2 subunit of voltage-gated calcium channels (VGCCs), as a developmental switch that limits axon growth and regeneration. Cacna2d2 gene deletion or silencing promoted axon growth in vitro. In vivo, Alpha2delta2 pharmacological blockade through Pregabalin (PGB) administration enhanced axon regeneration in adult mice after spinal cord injury (SCI)...
September 27, 2016: Neuron
Vladimir A Maisky, Olena P Mankivska, Andriy V Maznychenko, Oleh V Vlasenko, Olexandr V Dovgan', Eike D Schomburg, Heinz Steffens
The NADPH-diaphorase activity and Fos-immunoreactivity within the ventral horn of the lumbar spinal cord were studied in cats with acute unilateral myositis following injection of carrageenan into the m.m. gastrocnemius-soleus. In carrageenan-injected cats maximum in the mean number of intensely stained NADPH-diaphorase reactive (NADPH-dr) neurons was found in lamina VII (+100%) and VIII (+33%) of the contralateral ventral horn of the L6/L7 segments as compared with control animals. The maximumal level of Fos-immunoreactivity was registered in the same laminae with ipsilateral predominance (39...
September 27, 2016: Acta Histochemica
Noriko Isoo, Takae Ohno, Mutsumi Isowaki, Satoshi Fukuda, Naoyuki Murabe, Hiroaki Mizukami, Keiya Ozawa, Masayoshi Mishina, Masaki Sakurai
Neuronal plasticity is especially active in the young, during short windows of time termed critical periods, and loss of a critical period leads to functional limitations in the adults. The mechanism that governs the length of critical periods remains unknown. Here we show that levels of the NMDA receptor GluN2B subunit, which functions as a Ca(2+) channel, declines in spinal cord synapses toward the end of the critical period for activity-dependent corticospinal synapse elimination. This period could be prolonged by blocking the decline of GluN2B, and after its termination the critical period could be reopened through upregulation of GluN2B...
September 28, 2016: Scientific Reports
Marjorie Kerzoncuf, Laurent Bensoussan, Jean Michel Viton, Alain Delarque, Christiane Rossi Durand
OBJECTIVE: The therapeutic effects of intramuscular injections of botulinum toxin-type A on spasticity can be largely explained by its blocking action at the neuromuscular junction. BTx-A is assumed also to have a central action by affecting the functional organization of the CNS. The objective was to assess its action on spinal motor networks by investigating the post-activation depression (post-AD) of the soleus H-reflex in post-stroke patients. Post-AD that is a presynaptic mechanism controlling the synaptic efficacy of Ia-motoneuron transmission is involved in the pathophysiology of spasticity...
September 2016: Annals of Physical and Rehabilitation Medicine
Jiangbo Pu, Hanhui Xu, Yazhou Wang, Hongyan Cui, Yong Hu
Spinal cord injury (SCI) is a high-cost disability and may cause permanent loss of movement and sensation below the injury location. The chance of cure in human after SCI is extremely limited. Instead, neural regeneration could have been seen in animals after SCI, and such regeneration could be retarded by blocking neural plasticity pathways, showing the importance of neural plasticity in functional recovery. As an indicator of nonlinear dynamics in the brain, sample entropy was used here in combination with detrended fluctuation analysis (DFA) and Kolmogorov complexity to quantify functional plasticity changes in spontaneous EEG recordings of rats before and after SCI...
October 2016: Cognitive Neurodynamics
Gabriel Rusanescu, Jianren Mao
Unilateral peripheral nerve chronic constriction injury (CCI) has been widely used as a research model of human neuropathic pain. Recently, CCI has been shown to induce spinal cord adult neurogenesis, which may contribute to the chronic increase in nociceptive sensitivity. Here, we show that CCI also induces rapid and profound asymmetrical anatomical rearrangements in the adult rodent cerebellum and pons. This remodelling occurs throughout the hindbrain, and in addition to regions involved in pain processing, also affects other sensory modalities...
September 24, 2016: Journal of Cellular and Molecular Medicine
D P Fields, G S Mitchell
Spinal metabotropic serotonin receptors encode transient experiences into long-lasting changes in motor behavior (i.e. motor plasticity). While interactions between serotonin receptor subtypes are known to regulate plasticity, the significance of molecular divergence in downstream G protein coupled receptor signaling is not well understood. Here we tested the hypothesis that distinct cAMP dependent signaling pathways differentially regulate serotonin-induced phrenic motor facilitation (pMF); a well-studied model of spinal motor plasticity...
September 20, 2016: Neuropharmacology
Cheng-Yuan Lai, Yu-Cheng Ho, Ming-Chun Hsieh, Hsueh-Hsiao Wang, Jen-Kun Cheng, Yat-Pang Chau, Hsien-Yu Peng
UNLABELLED: Spinal plasticity, a key process mediating neuropathic pain development, requires ubiquitination-dependent protein turnover. Presynaptic active zone proteins have a crucial role in regulating vesicle exocytosis, which is essential for synaptic plasticity. Nevertheless, the mechanism for ubiquitination-regulated turnover of presynaptic active zone proteins in the progression of spinal plasticity-associated neuropathic pain remains unclear. Here, after research involving Sprague Dawley rats, we reported that spinal nerve ligation (SNL), in addition to causing allodynia, enhances the Rab3-interactive molecule-1α (RIM1α), a major active zone protein presumed to regulate neural plasticity, specifically in the synaptic plasma membranes (SPMs) of the ipsilateral dorsal horn...
September 14, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Sameer H Halani, Jonathan P Riley, Gustavo Pradilla, Faiz U Ahmad
Traumatic neurologic injury in contact sports is a rare but serious consequence for its players. These injuries are most commonly associated with high-impact collisions, for example in football, but are found in a wide variety of sports. In an attempt to minimize these injuries, sports are trying to increase safety by adding protection for participants. Most recently is the seemingly 'safe' sport of Bubble Soccer, which attempts to protect its players with inflatable plastic bubbles. We report a case of a 16-year-old male sustaining a cervical spine burst fracture with incomplete spinal cord injury while playing Bubble Soccer...
September 10, 2016: Journal of Clinical Neuroscience: Official Journal of the Neurosurgical Society of Australasia
Sara M F Turner, Darin J Falk, Barry J Byrne, David D Fuller
Pompe disease, caused by deficiency of acid alpha-glucosidase (GAA), leads to widespread glycogen accumulation and profound neuromuscular impairments. There has been controversy, however, regarding the role of central nervous system pathology in Pompe motor dysfunction. We hypothesized that absence of GAA protein causes progressive activation of neuropathological signaling, including pathways associated with cell death. To test this hypothesis, genomic data (Affymetrix Mouse Gene Array 2.0ST) from the mid-cervical spinal cord in 6- and 16-mo old Pompe (Gaa(-/-)) were evaluated (Broad Institute Molecular Signature Database), along with spinal cord histology...
September 9, 2016: Physiological Genomics
Itsaso Buesa, Zigor Aira, Jon Jatsu Azkue
Dopamine can influence NMDA receptor function and regulate glutamate-triggered long-term changes in synaptic strength in several regions of the CNS. In spinal cord, regulation of the threshold of synaptic plasticity may determine the proneness to undergo sensitization and hyperresponsiveness to noxious input. In the current study, we increased endogenous dopamine levels in the dorsal horn by using re-uptake inhibitor GBR 12935. During the so-induced hyperdopaminergic transmission, conditioning low-frequency (1 Hz) stimulation (LFS) to the sciatic nerve induced long-term potentiation (LTP) of C-fiber-evoked potentials in dorsal horn neurons...
2016: PloS One
Matilde Cordero-Erausquin, Perrine Inquimbert, Rémy Schlichter, Sylvain Hugel
The dorsal horn (DH) of the spinal cord receives a variety of sensory information arising from the inner and outer environment, as well as modulatory inputs from supraspinal centers. This information is integrated by the DH before being forwarded to brain areas where it may lead to pain perception. Spinal integration of this information relies on the interplay between different DH neurons forming complex and plastic neuronal networks. Elements of these networks are therefore potential targets for new analgesics and pain-relieving strategies...
September 3, 2016: Neuroscience
A Y Mushkin, E Y Malyarova, V A Evseev, P K Yablonskii
DESIGN: Case report. INTRODUCTION: The combination of severe post-infectious kyphosis and diaphragm relaxation is extremely rare in patient early than 1 year old. Its no publications concerning their simultaneous surgical treatment. CASE DESCRIPTION: 7-Month-old girl had simultaneous spinal reconstruction with anterior and posterior instrumentation and plastic of diaphragm because of sequelae of non-granulenatous spondylitis complicated by severe kyphosis (54°) and diaphragm relaxation...
2016: Neurologia i Neurochirurgia Polska
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