Plasticity In Central Nervous System Research Articles

The presence of a single-nucleotide polymorphism in the BDNF gene affects the rate of locomotor adaptation after stroke.

Induction of neural plasticity through motor learning has been demonstrated in animals and humans. Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family of growth factors, is thought to play an integral role in modulation of central nervous system plasticity during learning and motor skill recovery. Thirty percent of humans possess a single-nucleotide polymorphism on the BDNF gene (Val66Met), which has been linked to decreased activity-dependent release of BDNF. Presence of the polymorphism has been associated with altered cortical activation, short-term plasticity and altered skill acquisition, and learning in healthy humans. The impact of the Val66Met polymorphism on motor learning post-stroke has not been explored. The purpose of this study was to examine the impact of the Val66Met polymorphism in learning of a novel locomotor task in subjects with chronic stroke. It was hypothesized that subjects with the polymorphism would have an altered rate and magnitude of adaptation to a novel locomotor walking paradigm (the split-belt treadmill), compared to those without the polymorphism. The rate of adaptation was evaluated as the reduction in gait asymmetry during the first 30 (early adaptation) and last 100 (late adaptation) strides. Twenty-seven individuals with chronic stroke participated in a single session of split-belt treadmill walking and tested for the polymorphism. Step length and limb phase were measured to assess adaptation of spatial and temporal parameters of walking. The rate of adaptation of step length asymmetry differed significantly between those with and without the polymorphism, while the amount of total adaptation did not. These results suggest that chronic stroke survivors, regardless of presence or absence of the polymorphism, are able to adapt their walking pattern over a period of trial-and-error practice; however, the presence of the polymorphism influences the rate at which this is achieved.

Subventricular zone neural progenitors reverse TNF-alpha effects in cortical neurons.

IntroductionTumor necrosis factor alpha (TNFα) plays a physiological role in controlling synaptic transmission and plasticity in the healthy central nervous system by modulating glutamate receptor trafficking to the plasma membrane. TNFα expression is also rapidly induced in response to tissue injury and infection. By promoting the insertion of Ca2+ permeable-AMPA receptors into the neuronal plasma membrane, this cytokine may cause excessive Ca2+ influx into neurons, thus enhancing neuronal death.MethodsPrimary cultures of cortical neurons were obtained from E18 foetal mice and incubated for 24 h with adult neural stem cells (aNPCs) either stimulated with lipopolysaccharide (LPS+aNPCs) or not (aNPCs). Cultures were treated with TNFα (100 ng/ml), and electrophysiological recordings were performed in different conditions to evaluate the effect of the cytokine on neuronal transmission.ResultsIn this study, we demonstrate that aNPCs from the subventricular zone reverse the effects induced by the cytokine. Moreover, we show that the effect of aNPCs on cortical neurons is mediated by cannabinoid CB1 receptor activation.ConclusionThese data suggest that the role of aNPCs in preventing excitatory neurotransmission potentiation induced by TNFα on cortical neurons may have important implications for pathologies characterized by an inflammatory component affecting cortical neurons such as Alzheimer’s disease.Electronic supplementary materialThe online version of this article (doi:10.1186/s13287-015-0158-2) contains supplementary material, which is available to authorized users.

Stretch induced hyperexcitability of mice callosal pathway.

Memory and learning are thought to result from changes in synaptic strength. Previous studies on synaptic physiology in brain slices have traditionally been focused on biochemical processes. Here, we demonstrate with experiments on mouse brain slices that central nervous system plasticity is also sensitive to mechanical stretch. This is important, given the host of clinical conditions involving changes in mechanical tension on the brain, and the normal role that mechanical tension plays in brain development. A novel platform is developed to investigate neural responses to mechanical stretching. Flavoprotein autofluoresence (FA) imaging was employed for measuring neural activity. We observed that synaptic excitability substantially increases after a small (2.5%) stretch was held for 10 min and released. The increase is accumulative, i.e., multiple stretch cycles further increase the excitability. We also developed analytical tools to quantify the spatial spread and response strength. Results show that the spatial spread is less stable in slices undergoing the stretch-unstretch cycle. FA amplitude and activation rate decrease as excitability increases in stretch cases but not in electrically enhanced cases. These results collectively demonstrate that a small stretch in physiological range can modulate neural activities significantly, suggesting that mechanical events can be employed as a novel tool for the modulation of neural plasticity.

Single fluoxetine treatment before but not after stress prevents stress-induced hippocampal long-term depression and spatial memory retrieval impairment in rats.

A growing body of evidence has shown that chronic treatment with fluoxetine, a widely prescribed medication for treatment of depression, can affect synaptic plasticity in the adult central nervous system. However, it is not well understood whether acute fluoxetine influences synaptic plasticity, especially on hippocampal CA1 long-term depression (LTD), and if so, whether it subsequently impacts hippocampal-dependent spatial memory. Here, we reported that LTD facilitated by elevated-platform stress in hippocampal slices was completely prevented by fluoxetine administration (10 mg/kg, i.p.) 30 min before stress. The LTD was not, however, significantly inhibited by fluoxetine administration immediately after stress. Similarly, fluoxetine incubation (10 μM) during electrophysiological recordings also displayed no influence on the stress-facilitated LTD. In addition, behavioral results showed that a single fluoxetine treatment 30 min before but not after acute stress fully reversed the impairment of spatial memory retrieval in the Morris water maze paradigm. Taken together, these results suggest that acute fluoxetine treatment only before, but not after stress, can prevent hippocampal CA1 LTD and spatial memory retrieval impairment caused by behavioral stress in adult animals.

Microglia Function in Central Nervous System Development and Plasticity.

The nervous system comprises a remarkably diverse and complex network of different cell types, which must communicate with one another with speed, reliability, and precision. Thus, the developmental patterning and maintenance of these cell populations and their connections with one another pose a rather formidable task. Emerging data implicate microglia, the resident myeloid-derived cells of the central nervous system (CNS), in the spatial patterning and synaptic wiring throughout the healthy, developing, and adult CNS. Importantly, new tools to specifically manipulate microglia function have revealed that these cellular functions translate, on a systems level, to effects on overall behavior. In this review, we give a historical perspective of work to identify microglia function in the healthy CNS and highlight exciting new work in the field that has identified roles for these cells in CNS development, maintenance, and plasticity.

Developmental expression and localization of MHC class I molecules in the human central nervous system.

Recent animal studies have found neuronal expression of major histocompatibility complex (MHC) class I in the central nervous system (CNS). However, the developmental expression profiles of MHC class I in human CNS remain unclear. Here, we systemically evaluate the expression and subcellular localization of MHC class I molecules during human CNS development using immunohistochemistry and immunofluorescence. Between the age of 20-33 gestational weeks (GW), MHC class I expression was relatively absent in the cerebral cortex with the exception of a few neurons; however, expression increased rapidly in the cochlear nuclei and in the cerebellar cortical Purkinje cells while increasing slowly in the substantia nigra. Expression was also detected in some nuclei and nerve fibers of the brain stem including the ambiguus nucleus, the locus coeruleus and the solitary tract as early as 20 GW and persisted through 33 GW. These early-stage neural cells with MHC class I protein expression later developed neuronal morphology. 30-33 GW is an important period of MHC class I expression in neurons, and during this period, MHC class I molecules were found to be enriched not only in neuronal cell bodies and neurites but also in nerve fibers and in the surrounding stroma. No expression was detected in the adult brain with exception of the cerebrovascular endothelium. MHC class I molecules displayed greater postsynaptic colocalization in cerebellar Purkinje cells, in the lateral geniculate nucleus and in the cochlear nuclei. These results demonstrate diverse spatiotemporal expression patterns for MHC class I molecules in the prenatal human CNS and strongly support the notion that MHC class I molecules play important roles in both CNS development and plasticity.

New players in the mechanism of spinal cord stimulation for neuropathic pain

Abstract Aims The aim of this study was to uncover possible proteins involved in the mechanism for neuropathic spinal cord stimulation (SCS) pain relief in humans. Methods Using two different proteomic protocols we compared the protein concentration in cerebrospinal fluid (CSF) from 14 SCS responsive neuropathic pain patients using a shotgun proteomic approach. The comparison was made between samples from the same individual taken when the stimulator had been off for 48 h, and after the stimulator had been used as normal for three weeks. Mass spectrometry raw files from both experimental setups were analysed using MS Quant and DeCyder softwares and proteins were identified using MASCOT search against Swissprot database. After median normalization moderate paired t-test statistics were used in R limma package to find up-and down regulated proteins. Results In total, 255 and 216 proteins could be identified by the dimethyl and label free methods respectively and relatively quantified. Of these several were significantly up- and down regulated. Conclusions These novel proteins add to the SCS mechanism in patients with neuropathic pain. These results strengthen the evidence for SCS as altering extracellular matrix components and affecting central nervous system plasticity.

Repeated methylphenidate administration during lactation reduces maternal behavior, induces maternal tolerance, and increases anxiety-like behavior in pups in adulthood

Methylphenidate (MPD) is a dopamine uptake inhibitor and the most commonly prescribed drug for the treatment of attention-deficit/hyperactivity disorder in children. Several studies have shown that such stimulants as cocaine and amphetamine that are administered during gestation and lactation may disrupt maternal behavior. Also, MPD is used in lactation. Repeated MPD administration can induce either sensitization or tolerance. The aim of the present study was to investigate whether repeated MPD administration alters maternal behavior and promotes tolerance or sensitization in these females. The effects in adult offspring were also examined in models of anxiety. Methylphenidate (5mg/kg) was administered from lactation day 2 to 4, and maternal pup retrieval behavior was assessed. This treatment was continued until lactation day 7. At weaning, the dams received a challenge dose of MPD, and general activity was evaluated in the open field. Striatal monoamine and metabolite levels were also measured to determine whether this treatment promotes behavioral or biochemical plasticity. The long-term behavioral effects of MPD exposure were evaluated in pups in adulthood. The results showed an increase in the latency to retrieve the first, second, and third pups and a decrease in the number of dams that retrieved all pups. After a challenge dose of MPD, the dams exhibited a decrease in locomotion frequency, an increase in immobility duration in the open field, and a decrease in striatal serotonin levels. In pups, anxiety-like behavior increased in the light/dark box test. These results indicate that repeated MPD administration during early lactation impairs maternal behavior, likely by decreasing maternal motivation. Repeated MPD administration induced maternal tolerance at weaning after a challenge dose of MPD, suggesting the development of central nervous system plasticity. In pups, maternal exposure to MPD during early lactation induced long-term effects and increased anxiety-like behavior in adulthood.

Epigenetic modulation of brain gene networks for cocaine and alcohol abuse.

Cocaine and alcohol are two substances of abuse that prominently affect the central nervous system (CNS). Repeated exposure to cocaine and alcohol leads to longstanding changes in gene expression, and subsequent functional CNS plasticity, throughout multiple brain regions. Epigenetic modifications of histones are one proposed mechanism guiding these enduring changes to the transcriptome. Characterizing the large number of available biological relationships as network models can reveal unexpected biochemical relationships. Clustering analysis of variation from whole-genome sequencing of gene expression (RNA-Seq) and histone H3 lysine 4 trimethylation (H3K4me3) events (ChIP-Seq) revealed the underlying structure of the transcriptional and epigenomic landscape within hippocampal postmortem brain tissue of drug abusers and control cases. Distinct sets of interrelated networks for cocaine and alcohol abuse were determined for each abusive substance. The network approach identified subsets of functionally related genes that are regulated in agreement with H3K4me3 changes, suggesting cause and effect relationships between this epigenetic mark and gene expression. Gene expression networks consisted of recognized substrates for addiction, such as the dopamine- and cAMP-regulated neuronal phosphoprotein PPP1R1B/DARPP-32 and the vesicular glutamate transporter SLC17A7/VGLUT1 as well as potentially novel molecular targets for substance abuse. Through a systems biology based approach our results illustrate the utility of integrating epigenetic and transcript expression to establish relevant biological networks in the human brain for addiction. Future work with laboratory models may clarify the functional relevance of these gene networks for cocaine and alcohol, and provide a framework for the development of medications for the treatment of addiction.

Electroacupuncture analgesia is associated with increased serum brain-derived neurotrophic factor in chronic tension-type headache: a randomized, sham controlled, crossover trial.

BackgroundChronic tension-type headache (CTTH) is characterized by almost daily headaches and central sensitization, for which electroacupuncture (EA) might be effective. The central nervous system (CNS) plasticity can be tracked in serum using the brain-derived neurotrophic factor (BDNF), a neuroplasticity mediator. Thus, we tested the hypothesis that EA analgesia in CTTH is related to neuroplasticity indexed by serum BDNF.MethodsWe enrolled females aged 18–60 years with CTTH in a randomized, blinded, placebo-controlled crossover trial, comparing ten EA sessions applied for 30 minutes (2–10 Hz, intensity by tolerance) in cervical areas twice per week vs. a sham intervention. Treatment periods were separated by two washout weeks. Pain on the 10-cm visual analog scale (VAS) and serum BDNF were assessed as primary outcomes.ResultsThirty-four subjects underwent randomization, and twenty-nine completed the protocol. EA was superior to sham to alleviate pain (VAS scores 2.38 ± 1.77 and 3.02 ± 2.49, respectively, P = 0.005). The VAS scores differed according to the intervention sequence, demonstrating a carryover effect (P < 0.05). Using multiple regression, serum BDNF was adjusted for the Hamilton depression rating scale (HDRS) and the VAS scores (r-squared = 0.07, standard β coefficients = −0.2 and −0.14, respectively, P < 0.001). At the end of the first intervention period, the adjusted BDNF was higher in the EA phase (29.31 ± 3.24, 27.53 ± 2.94 ng/mL, Cohen’s d = 0.55).ConclusionEA analgesia is related to neuroplasticity indexed by the adjusted BDNF. EA modulation of pain and BDNF occurs according to the CNS situation at the moment of its administration, as it was related to depression and the timing of its administration.

Experimental Advances Towards Neural Regeneration from Induced Stem Cells to Direct In Vivo Reprogramming.

Neuronal loss is a common substrate of many neurological diseases that still lack effective treatments and highly burden lives of affected individuals. The discovery of self-renewing stem cells within the central nervous system (CNS) has opened the doors to the possibility of using the plasticity of CNS as a potential strategy for the development of regenerative therapies after injuries. The role of neural progenitor cells appears to be crucial, but insufficient in reparative processes after damage. In addition, the mechanisms that regulate these events are still largely unknown. Stem cell-based therapeutic approaches have primarily focused on the use of either induced pluripotent stem cells or induced neural stem cells as sources for cell transplantation. More recently, in vivo direct reprogramming of endogenous CNS cells into multipotent neural stem/progenitor cells has been proposed as an alternative strategy that could overcome the limits connected with both the invasiveness of exogenous cell transplantation and the technical issues of in vitro reprogramming (i.e., the time requested and the limited available amount of directly induced neuronal cells). In this review, we aim to highlight the recent studies on in vivo direct reprogramming, focusing on astrocytes conversion to neurons or to neural stem/precursors cells, in the perspective of future therapeutic purposes for neurological disorders.

PP01.4 – 2720: Novel mutation in GRIN1 gene expressed as neonatal-onset drug-resistant epilepsy associated with microcephaly and polymicrogyria

Objective A male infant with severe psychomotor retardation, congenital progressive microcephaly who presented in the first week of life with intractable neonatal seizures underwent genetic analysis. Brain MRI showed migration and sulcation disorder of the gray matter associated with bilateral fronto-parietal and temporal polymicrogyria. Genes mutations associated with abnormal cortical migration (such as CDX, LIS1, ARX, TUBBB1A, TUBB2A, TUBB2B, WDR62 and GPR56) were not detected. Methods Whole exome sequencing was employed and revealed 20,149 changes. Analysis of these mutations, filtration of nonspecific mutations and separation of alterations that were not present in the DNA samples of his parents provided us with one heterozygous mutation. Results We detected a novel mutation (c.2365 G> A p. D789N) in the GRIN1 gene. No single nucleotide polymorphisms were found in this region and its probability score was 1.0. The GRIN1 gene encodes the subunit 1 of the N-methyl D-aspartate (NMDA) ionotropic glutamate receptor which has an excitatory effect that may control synaptic plasticity in the central nervous system. Conclusion GRIN1 mutations were previously reported in children with “idiopathic” epilepsy, non-syndromic intellectual disabilities and recently with epileptic encephalopathy (such as infantile spasms) but not with malformations of cortical migration. The present report expands the clinical spectrum of GRIN1-associated neurological disorders, and suggests that early fetal NMDAR-induced exitotoxicity (during the late neuronal migration period) underlies neuronal damage which lead to microcephaly, polymicrogyria and intractable epilepsy.

Notch signaling activation is critical to the development of neuropathic pain.

BackgroundNerve injury-induced neuropathic pain is a major health problem worldwide. Notch signaling is a highly conserved pathway in evolution, which has an important role in synaptic plasticity and inflammation in central nervous system. The present study was designed to investigate the potential role of notch signaling in the development of neuropathic pain.MethodsThe neuropathic pain was induced by spared nerve injury (SNI) in rats. The activation of notch signaling in the lumbar spinal dorsal horn was measured. DAPT, an inhibitor of notch signaling, was intrathecally (i.t.) administered before SNI or after appearance of pain sensitivity. Moreover, Jagged-1 (JAG-1) peptide, a ligand of notch signaling, was i.t. administered to normal rats. The mechanical allodynia was assessed by von Frey test.ResultsHere, we found that DAPT administered 0.5 h before SNI operation could significantly prevent the decrease of mechanical paw withdrawal threshold (PWT) for more than 4 weeks (P < 0.05 vs. SNI group). DAPT administered after appearance of pain sensitivity could also significantly reverse the decrease of mechanical PWT in a dose-dependent manner (P < 0.05). In addition, administration of Jagged-1 (JAG-1) peptide significantly decreased the mechanical PWT of normal rats in a dose-dependent manner (P < 0.05).ConclusionsTherefore, notch signaling activation might contribute to the development of neuropathic pain. This study might provide a new therapeutic target for neuropathic pain.

Recombinant Nogo-66 via soluble expression with SUMO fusion in Escherichia coli inhibits neurite outgrowth in vitro.

Nogo-66, a hydrophilic loop of 66 amino acids flank two hydrophobic domains of the Nogo-A C terminus, interacts with the Nogo-66 receptor (NgR) to exert numerous functions in the central nervous system (CNS). Nogo-66 has important roles in aspects of neuronal development, including cell migration, axon guidance, fasciculation, and dendritic branching, and in aspects of CNS plasticity, including oligodendrocyte differentiation and myelination. Here, the small ubiquitin-related modifier (SUMO) was fused to the target gene, Nogo-66, and the construct was expressed in Escherichia coli (E. coli). Under the optimal fermentation conditions, the soluble expression level of the fusion protein was 33 % of the total supernatant protein. After cleaving the fusion proteins with SUMO protease and purifying them by Ni-NTA affinity chromatography, the yield and purity of recombinant Nogo-66 obtained by 10-L scale fermentation were 23 ± 1.5 mg/L and greater than 93 %, respectively. The authenticity of the recombinant Nogo-66 was confirmed by an electrospray ionization-mass spectrometry analysis. The functional analyses indicated that the recombinant Nogo-66 was capable of binding the NgR specifically. The immunofluorescence results showed that the recombinant Nogo-66 could significantly inhibit neurite outgrowth of rat pheochromocytoma (PC12) cells stimulated by nerve growth factor and cerebellar granule cells (CGCs). Furthermore, Nogo-66 inhibited neurite outgrowth by increasing the level of phosphorylated Rho-associated coiled-coil-containing protein kinase 2 (ROCK2), collapsin response mediator protein 2 (CRMP2), and myosin light chain (MLC). This study provided a feasible and convenient production method for generating sufficient recombinant Nogo-66 for experimental and clinical applications.

22. Plasticity of sensorimotor system induced by sustained pressure stimulation

Introduction The aim of this study was to assess functional changes occurring at central nervous system (CNS) in healthy volunteers after sustained pressure stimulation according to Vojta (Bauer et al., 1992), a physiotherapeutic method involving induction of a complex motor response, so called reflex locomotion. Although the therapy has been widely used in clinical practice, its underlying neurobiological basis remains a speculation. We hypothesize that the stimulation-driven response induces CNS plasticity at subcortical level detectable by functional magnetic resonance imaging (fMRI), possibly involving specific changes in task-related sensorimotor system activation as well as modulation of resting state networks. Methods Two groups of healthy volunteers were included (17 females and 5 males in each group, mean age 24.5 and 24.7 respectively): Group A receiving stimulation at the Vojta right heel zone and Group B receiving control stimulation of the right ankle. All subjects underwent a single fMRI session using a 1.5T Siemens scanner, including 6 experimental runs employing 3 different conditions: rest (6min); dominant hand finger tapping alternating with rest (6min); intermittent pressure stimulation applied by an experienced therapist (10min). Both rest and finger tapping conditions were tested before and after two consecutive stimulation runs. Statistical analysis, including standard pre-processing, nuisance signal regression and group post hoc contrasts, was carried out using FEAT, and MELODIC followed by Dual Regression, parts of FSL (Jenkinson et al., 2012) 5.0. The resulting statistical maps were thresholded at corrected significance level p Results In finger tapping task, diffuse activation decrease within sensorimotor system was observed in both groups. However, there was significant activation increase mainly in motor nuclei of left thalamus detected only in group A. Additionally, group A showed significant decrease of functional connectivity in the left superior parietal lobule within the bilateral sensorimotor resting-state network. Conclusions Our findings provide evidence that stimulation according to Vojta is associated with specific and persistent changes of brain activation, as compared to the control stimulation. The observed changes could represent neurophysiological correlate of Vojta therapy and suggest an important role of subcortical structures. Acknowledgement Supported by grant GACR 14–22572S.

NO‐ting a putative mechanism by which anti‐migraine drugs mitigate trigeminal neuropathic pain

<scp>NO</scp>‐ting a putative mechanism by which anti‐migraine drugs mitigate trigeminal neuropathic pain

Neuroplasticity underlying the comorbidity of pain and depression.

Acute pain induces depressed mood, and chronic pain is known to cause depression. Depression, meanwhile, can also adversely affect pain behaviors ranging from symptomology to treatment response. Pain and depression independently induce long-term plasticity in the central nervous system (CNS). Comorbid conditions, however, have distinct patterns of neural activation. We performed a review of the changes in neural circuitry and molecular signaling pathways that may underlie this complex relationship between pain and depression. We also discussed some of the current and future therapies that are based on this understanding of the CNS plasticity that occurs with pain and depression.

Do pursuit movement tasks lead to differential changes in early somatosensory evoked potentials related to motor learning compared with typing tasks?

Central nervous system (CNS) plasticity is essential for development; however, recent research has demonstrated its role in pathology, particularly following overuse and repetition. Previous studies investigating changes in sensorimotor integration (SMI) have used relatively simple paradigms resulting in minimal changes in neural activity, as determined through the use of somatosensory evoked potentials (SEPs). This study sought to utilize complex tasks and compare separate motor paradigms to determine which one best facilitates long-term learning. Spinal, brainstem, and cortical SEPs were recorded following median nerve stimulation at the wrist pre- and postinterventions. Eighteen participants performed the same paradigms, a control condition of 10 min of mental recitation and two interventions, one consisting of 10 min of tracing and the other 10 min of repetitive typing. Significant increases in the N13, N20, P25, and N30 SEP peaks were seen for both interventions. A significant decrease in the N24 SEP peak was observed for both interventions. Significant improvements in accuracy were seen for both interventions postacquisition but only for tracing during retention. The changes seen following motor learning were congruent with those associated with long-term learning, which was also reflected by significant increases in accuracy during retention. Tracing or the pursuit movement paradigm was shown to be a more effective learning tool. The identification of a task that is sufficiently novel and complex, leading to robust changes in SEP peaks, indicates a task that can be utilized in future work to study clinical populations and the effect of experimental interventions on SMI.

Anatomy, physiology and neurobiology of the nociception: A focus on low back pain (part A)

IntroductionThe treatment of Failed Back Surgery Syndrome (FBSS) remains a challenge for pain medicine due to the complexity in the interactions between [1] a residual mechanical pain after surgery and, [2] a progressive transition into chronic pain involving central nervous system plasticity and molecular reorganization. The aim of this paper is to provide a fundamental overview of the pain pathway supporting the nociceptive component of the back pain. MethodsLiterature searches included an exhaustive review of 643 references and 74 book chapters updated by searching the major electronic databases from 1930 to August 2013. ResultsPain input is gathered by the peripheral fibre from the innervated tissue's environment and relayed by two contiguous central axons to the brain, via the spinal cord. At this level, it is possible to characterize physical pain and emotional pain. These are supported by two different pathways, encoding two dimensions of pain perception: In Neo-spino-thalamic pathway, the wide dynamic range neuron system is able to provide the information needed for mapping the “sensory-discriminative” dimension of pain. The second projection system (Paleo-spino-thalamic pathway) also involves the ventromedial thalamus but projects to the amygdala, the insula and the anterior cingulate cortex. These areas are associated with emotionality and affect. ConclusionThe mechanical component of FBSS cannot be understood unless the functioning of the pain system is known. But ultimately, the highly variable nature of back pain expression among individuals would require a careful pathophysiological dissection of the potential generators of back pain to guide pain management strategies.

Sport practice and stress management in French soldiers deployed in Afghanistan: Is sport dependence a risk factor for psychological distress?

IntroductionSport activities can be considered either in terms of sport consumption or sport dependence characterizing a behavioral addiction [1–3]. The objective of this study concerned the effects of exercise-induced sport dependence on soldiers stress resistance in the context of a six months deployment in Afghanistan.MethodsIn an anonymous prospective cohort study we assessed before during and six months after deployment Extra Regimental Sport consumption (ERS), exercise dependence (ED; 2,5), anxiety and depression diseases, perceived stress, and mood of Tension/Anxiety. Plasmatic Brain Derived Neurotrophic Factor (BDNF), considered as a good marker of central nervous system plasticity, was assessed before and after.ResultsAmong the 397 young soldiers evaluated before and during the deployment, 131 had been assessed six months after. Before deployment, 65% of soldiers have ERS consumption. 42% presented ED, which was not related with higher ERS consumption. Levels of perceived stress, anxiety and depression diseases were higher for ED subjects and were not influenced by ERS consumption. In soldiers without ED, perceived stress and mood of tension/anxiety were higher in subjects without ERS. Neither ERS consumption, nor ED altered BDNF concentration. During deployment, the percentage of ED was not modified, but the distribution in sport dependence group was modified: 64% of soldiers with ED were not identified as addicted before. After 3 months, soldiers presenting ED had a higher Mood of tension/anxiety level. After deployment, both a higher BDNF concentration and anxiety disease score were observed in soldiers developing ED refer to those who did not develop ED.DiscussionED seems to present: (1) a relation with a high “anxiety”, (2) a liability in chronic stress environment. However, ED could be considered as an efficient strategy referred to the high level of BDNF after the mission. A follow-up is ongoing 18 months after the deployment to confirm this assumption.