Injection Of Hypertonic Saline Research Articles

The effect of experimentally-induced subacromial pain on proprioception

Shoulder injuries may be associated with proprioceptive deficits, however, it is unknown whether these changes are due to the experience of pain, tissue damage, or a combination of these. The aim of this study was to investigate the effect of experimentally-induced sub-acromial pain on proprioceptive variables. Sub-acromial pain was induced via hypertonic saline injection in 20 healthy participants. Passive joint replication (PJR) and threshold to detection of movement direction (TTDMD) were assessed with a Biodex System 3 Pro isokinetic dynamometer for baseline control, experimental pain and recovery control conditions with a starting position of 60° shoulder abduction. The target angle for PJR was 60° external rotation, starting from 40°. TTDMD was tested from a position of 20° external rotation. Repeated measures ANOVAs were used to determine differences between PJR absolute and variable errors and TTDMD for the control and experimental conditions. Pain was elicited with a median 7 on the Numeric Pain Rating Scale. TTDMD was significantly decreased for the experimental pain condition compared to baseline and recovery conditions (≈30%, P = 0.003). No significant differences were found for absolute (P = 0.152) and variable (P = 0.514) error for PJR. Movement sense was enhanced for the experimental sub-acromial pain condition, which may reflect protective effects of the central nervous system in response to the pain. Where decreased passive proprioception is observed in shoulders with injuries, these may be due to a combination of peripheral tissue injury and neural adaptations that differ from those due to acute pain.

Effects of endogenous nesfatin-1 on drinking behavior of rats

Objective To explore the effect of nesfatin-1 on water intake and the mechanism of nesfatin-1 in regulating water and electrolyte balance in hypothalamus of rats. Methods Lateral ventricle implantation tube, drugs and molecular biology were used to observe the effects of exogenous and endogenous nesfatin-1 on water intake in drug causing thirsty rats and on physiological thirsty rats. Meanwhile the gene expression of NUCB2/Nesfatin-1 of water ban rats has been observed. Results Lateral ventricle injection of 150, 450 pmol exogenous nesfatin-1, the water intake in 0-120 min of rats significantly reduced (150 pmol(1.3±0.2)-(1.85±0.3)ml/100g; 450 pmol(0.8±0.4)-(1.2±0.4)ml/100g vs NS(2.5±0.3)-(3.1±0.2)ml/100g) and showed a significant dose-response relationship (P 0.05). Angiotensin II were administrated to lateral ventricle 10 min after injection of nesfatin-1. After injection of 150 pmol nesfatin-1, water intake in 15-30 min of rats significantly reduced (150 pmol(2.17±0.6)ml/100g vs NS(3.62 ±1.0)ml/100g, P 0.05). Subcutaneous injection of hypertonic saline, and water intake in rats increase rapidly(The water intake of rats with subcutaneous injection of hypertonic saline increase rapidly, while the water intake of rats with 150 pmol nesfatin-1 injection in lateral ventricle within 15~30 min and the water intake of rats with 450 pmol nesfatin-1 injection in lateral ventricle within 120 min significantly reduced. Lateral ventricle injection of 150 or 450 pmol nesfatin-1, water intake of each time period within 60 min in rats significantly reduced (150 pmol : (0.25±0.2)-(1.6±0.25)ml/100g; 450 pmol(0.1±0.15)-(1.92±0.2)ml/100g vs NS(0.9±0.2)-(2.9±0.2)ml/100g , P 0.05). Three hours After the second time hypothalamus PVN injection of antisense RNA nesfatin-1, angiotensin II (50 pmol/2 mul) were given and water intake in rats increased significantly (Antisense nesfatin-1(1.87±0.4)-(2.77±0.6)ml/100g vs NS(0.72±0.1)-(1.17±0.4)ml/100g , P 0.05). NUCB2 gene expression was significantly reduced in the hypothalamus (water ban: (-7.2±1.1)% vs free drinking water: (0.82±0.4)%, P<0.01) in rats after 18 hours water ban; The hypothalamus NUCB2 gene expression had a significant rise (water supply restore: (8.1±1.1)% vs free drinking water: (0.82±0.4)%, P<0.01) in rats with water supply restore. Conclusion Nesfatin-1 involves in the regulation of water intake in physiology or drug causing thirsty. Nesfatin-1 plays an important role in the hypothalamus to regulate water-electrolyte balance and thirsty mechanisms. Key words: Nesfatin-1; Drinking behaviour; Angiotensin II; Rat

Potential interaction of experimental knee pain and laterally wedged insoles for knee off-loading during walking

BackgroundLaterally wedged insoles are one of the gait modifications potentially slowing down progression of medial knee osteoarthritis. Clinical studies have, however, found large individual differences in the biomechanical effect and an insufficient pain reduction. To clarify if and how pain mediates mechanical changes during gait the current study investigated how acute experimental knee pain changes the mechanical effect of laterally wedged insoles in healthy subjects during walking. Methods3D gait analysis was carried out for twelve healthy individuals. The study followed a cross-over design and data were collected with both a neutral and a 10-degree laterally wedged insole with experimental pain induced by hypertonic and isotonic saline injections into the infrapatellar fat pad. Peak knee adduction moment was the primary outcome. A repeated ANOVA (analysis of variance) was used to evaluate the relationship between the factors wedge, condition and test number. FindingsWedges significantly reduced peak knee adduction moment but experimental knee pain did only marginally affect its magnitude in either condition. While frontal plane mechanics were relatively unaffected by pain, the sagittal plane knee extension moment increased with laterally wedging (P=0.008), whereas late knee flexion moment was reduced by experimental knee pain (P=0.04). InterpretationThe effect of laterally wedged insoles in attenuating knee adduction moment during walking is independent of experimental knee pain. The present study provides evidence that subjects with experimental knee pain reduce knee loading by reducing extension moment, whereas lateral wedges have the opposite effect and increase the extension moment.

In vivo experimental study on the effects of fluid in increasing the efficiency of radiofrequency ablation.

Radiofrequency ablation (RFA) is the most widely used and studied method internationally for the local treatment of liver tumors. However, the extension of coagulation necrosis in one RFA procedure is limited and incomplete coverage of the damaged area can lead to a high local recurrence rate. In this study, we compared the effects of different solutions in enhancing hepatic radiofrequency by establishing a rabbit VX2 liver cancer model. We also determined the optimal solution to maximise effects on the extent of RFA-induced coagulation necrosis. Thirty VX2 tumor rabbits were randomly assigned to five groups: group A, RFA alone; group B, RFA with anhydrous ethanol injection; group C, RFA with 5% hypertonic saline injection; group D, RFA with lidocaine injection; and group E, RFA with a mixed solution. Routine ultrasound examinations and contrast-enhanced ultrasound (CEUS) of the ablation areas were performed after RFA. Then, we measured the major axis and transverse diameter and compared the areas of coagulation necrosis induced by RFA. The mean ablation area range increased in groups B, C and especially E, and the scopes were greater compared with group A. Preoperative application of anhydrous ethanol, hypertonic saline, lidocaine and the mixed solution (groups B, C, D and E, respectively) resulted in larger coagulation necrosis areas than in group A (p<0.05). Among the groups, the coagulation necrosis areas in group E was largest, and the difference was statistically significant compared with other groups (p<0.05). Pathological findings were consistent with imaging results. A mixture of dehydrated alcohol, hypertonic saline and lidocaine injected with RFA increases the extent of coagulation necrosis in the liver with a single application, and the mixed solution is more effective than any other injection alone.

Jaw-opening accuracy is not affected by masseter muscle vibration in healthy men.

There is a functional integration between the jaw and neck regions with head extension-flexion movements during jaw-opening/closing tasks. We recently reported that trigeminal nociceptive input by injection of hypertonic saline into the masseter muscle altered this integrated jaw-neck function during jaw-opening/closing tasks. Thus, in jaw-opening to a predefined position, the head-neck component increased during pain. Previous studies have indicated that muscle spindle stimulation by vibration of the masseter muscle may influence jaw movement amplitudes, but the possible effect on the integrated jaw-neck function is unknown. The aim of this study was to investigate the effect of masseter muscle vibration on jaw-head movements during a continuous jaw-opening/closing task to a target position. Sixteen healthy men performed two trials without vibration (Control) and two trials with bilateral masseter muscle vibration (Vibration). Movements of the mandible and the head were registered with a wireless three-dimensional optoelectronic recording system. Differences in jaw-opening and head movement amplitudes between Control and Vibration, as well as achievement of the predefined jaw-opening target position, were analysed with Wilcoxon's matched pairs test. No significant group effects from vibration were found for jaw or head movement amplitudes, or in the achievement of the target jaw-opening position. A covariation between the jaw and head movement amplitudes was observed. The results imply a high stability for the jaw motor system in a target jaw-opening task and that this task was achieved with the head-neck and jaw working as an integrated system.

Pain reported during prolonged standing is associated with reduced anticipatory postural adjustments of the deep abdominals.

Within the context of low back pain, the measurement of deep abdominal anticipatory postural adjustments (APAs) during rapid limb movement has received much interest. There is dispute about the association between APAs and back pain. Moreover, there is limited evidence examining compensatory postural adjustments (CPAs) in back pain. This study examined the relationship between APAs and CPAs with pain reported in the low back during 2 h of prolonged standing. Twenty-six participants with no history of severe back pain performed 2-h prolonged standing. APAs and CPAs of the deep abdominal muscles (transverse abdominis/internal obliques) were measured by surface electromyography during rapid shoulder flexion and extension. APAs and CPAs measured pre-standing revealed symmetrical anticipatory activity, but an asymmetry between the different sides of the abdominal wall for CPAs. APAs and CPAs measured pre-standing were not associated with pain reported during standing. For the whole group, APA amplitudes were reduced post-standing during shoulder flexion (p = 0.005). Pain reported during standing was associated with the changes in APA amplitudes post-standing (rs = 0.43, p = 0.002). These findings support previous research using hypertonic saline injections to induce back pain that showed reduced APA amplitudes, and extends findings to suggest pain does not effect compensatory postural adjustments.

Roux-en-Y gastric bypass does not affect daily water intake or the drinking response to dipsogenic stimuli in rats.

Bariatric surgery is currently the most effective treatment for severe obesity, and Roux-en-Y gastric bypass (RYGB) is the most common approach in the United States and worldwide. Many studies have documented the changes in body weight, food intake, and glycemic control associated with the procedure. Although dehydration is commonly listed as a postoperative complication, little focus has been directed to testing the response to dipsogenic treatments after RYGB. Accordingly, we used a rat model of RYGB to test for procedure-induced changes in daily water intake and in the response to three dipsogenic treatments: central administration of ANG II, peripheral injection of hypertonic saline, and overnight water deprivation. We did not find any systematic differences in daily water intake of sham-operated and RYGB rats, nor did we find any differences in the response to the dipsogenic treatments. The results of these experiments suggest that RYGB does not impair thirst responses and does not enhance any satiating effect of water intake. Furthermore, these data support the current view that feedback from the stomach is unnecessary for the termination of drinking behavior and are consistent with a role of orosensory or postgastric feedback.

Laparoscopic rectopexy for external prolapse in children

PurposeThis study reports the results of laparoscopic rectopexy in children. MethodsResults were obtained from a prospective database for all laparoscopic rectopexy procedures performed for external prolapse in a tertiary referral centre from 2006 to 2013. Outcomes included recurrence of symptoms and/or visible prolapse as well as the need for further surgery ResultsEighteen procedures including both suture and mesh rectopexy were performed in 11 patients. Six had solitary rectal ulcers. All patients had failed conservative management, including laxative therapy, and one patient had previously had a trial of injection of hypertonic saline. At a median follow up of 33months (6–75) complete resolution was seen in 7 cases and partial resolution, with some continuing symptoms, was seen in 1 patient. All suture rectopexy cases ultimately failed and required a redo rectopexy procedure. Three patients had persistent failure with recurrence of prolapse during the study period despite repeated procedures. There were no serious complications. ConclusionsLaparoscopic mesh rectopexy can be safely performed in children and can lead to complete resolution of external prolapse. There is a cohort for whom it fails to relieve the problem. In this series there was a trend towards less recurrence with mesh rectopexy.

Task dependency of motor adaptations to an acute noxious stimulation

This study explored motor adaptations in response to an acute noxious stimulation during three tasks that differed in the number of available degrees of freedom. Fifteen participants performed three isometric force-matched tasks (single leg knee extension, single leg squat, and bilateral leg squat) in three conditions (Control, Pain, and Washout). Pain was induced by injection of hypertonic saline into the vastus medialis muscle (VM; left leg). Supersonic shear imaging was used to measure muscle shear elastic modulus as this is considered to be an index of muscle stress. Surface electromyography (EMG) was recorded bilaterally from six muscles to assess changes in neural strategies. During tasks with fewer degrees of freedom (knee extension and single leg squat task), there was no change in VM EMG amplitude or VM shear elastic modulus. In contrast, during the bilateral leg squat, VM (-32.9 ± 15.8%; P < 0.001) and vastus lateralis (-28.7 ± 14.8%; P < 0.001) EMG amplitude decreased during Pain. This decrease in activation was associated with reduced VM shear elastic modulus (-17.6 ± 23.3%; P = 0.029) and reduced force produced by the painful leg (-10.0 ± 10.2%; P = 0.046). This work provides evidence that when an obvious solution is available to decrease stress on painful tissue, this option is selected. It confirms the fundamental assumption that motor adaptations to pain aim to alter load on painful tissue to protect for further pain and/or injury. The lack of adaptation observed during force-matched tasks with fewer degrees of freedom might be explained by the limited potential to redistribute stress or a high cost induced by such a compensation.

Electromyographic response of shoulder muscles to acute experimental subacromial pain

This study investigated effects of experimentally-induced subacromial pain, induced via hypertonic saline injection, on shoulder muscles activity. Electromyographic activity of 20 healthy participants was assessed for humeral elevation and descent for the control and experimental pain conditions, using fine wire electrodes for subscapularis and supraspinatus and surface electrodes for middle deltoid, upper trapezius, lower trapezius, infraspinatus, and serratus anterior. Normalized mean amplitudes were analyzed for each muscle for four phases for elevation and descent, respectively. Repeated measures analysis of variances (ANOVAs) were used to determine differences between muscle activity in the control and experimental condition for the four phases of elevation and descent. Differences for mean normalized amplitudes were not significant during humeral elevation. Increased activity was found for the pain condition for serratus anterior and middle deltoid during the first (120–90°) and third (60–30°) parts and decreased activity for infraspinatus in the second half of descent (60–0°). No significant differences were found during descent for upper and lower trapezius, subscapularis and supraspinatus. While increased serratus anterior activity during 60–30° of descent may be protective, increased middle deltoid and decreased infraspinatus activity during the same range may threaten subacromial tissues in that range. Overall the changes in muscle activation were individual specific, particularly during the concentric elevation phase.

Extracellular signal‐regulated kinase phosphorylation in forebrain neurones contributes to osmoregulatory mechanisms

Vasopressin secretion from the magnocellular neurosecretory cells (MNCs) is crucial for body fluid homeostasis. Osmotic regulation of MNC activity involves the concerted modulation of intrinsic mechanosensitive ion channels, taurine release from local astrocytes as well as excitatory inputs derived from osmosensitive forebrain regions. Extracellular signal-regulated protein kinases (ERK) are mitogen-activated protein kinases that transduce extracellular stimuli into intracellular post-translational and transcriptional responses, leading to changes in intrinsic neuronal properties and synaptic function. Here, we investigated whether ERK activation (i.e. phosphorylation) plays a role in the functioning of forebrain osmoregulatory networks. We found that within 10min after intraperitoneal injections of hypertonic saline (3m, 6m) in rats, many phosphoERK-immunopositive neurones were observed in osmosensitive forebrain regions, including the MNC containing supraoptic nuclei. The intensity of ERK labelling was dose-dependent. Reciprocally, slow intragastric infusions of water that lower osmolality reduced basal ERK phosphorylation. In the supraoptic nucleus, ERK phosphorylation predominated in vasopressin neurones vs. oxytocin neurones and was absent from astrocytes. Western blot experiments confirmed that phosphoERK expression in the supraoptic nucleus was dose dependent. Intracerebroventricular administration of the ERK phosphorylation inhibitor U 0126 before a hyperosmotic challenge reduced the number of both phosphoERK-immunopositive neurones and Fos expressing neurones in osmosensitive forebrain regions. Blockade of ERK phosphorylation also reduced hypertonically induced depolarization and an increase in firing of the supraoptic MNCs recorded in vitro. It finally reduced hypertonically induced vasopressin release in the bloodstream. Altogether, these findings identify ERK phosphorylation as a new element contributing to the osmoregulatory mechanisms of vasopressin release.

5-HT neurons of the area postrema become c-Fos-activated after increases in plasma sodium levels and transmit interoceptive information to the nucleus accumbens.

Serotonergic (5-hydroxytryptamine, 5-HT) neurons of the area postrema (AP) represent one neuronal phenotype implicated in the regulation of salt appetite. Tryptophan hydroxylase (Tryp-OH, synthetic enzyme-producing 5-HT) immunoreactive neurons in the AP of rats become c-Fos-activated following conditions in which plasma sodium levels are elevated; these include intraperitoneal injections of hypertonic saline and sodium repletion. Non-Tryp-OH neurons also became c-Fos-activated. Sodium depletion, which induced an increase in plasma osmolality but caused no significant change in the plasma sodium concentration, had no effect on the c-Fos activity in the AP. Epithelial sodium channels are expressed in the Tryp-OH-immunoreactive AP neurons, possibly functioning in the detection of changes in plasma sodium levels. Since little is known about the neural circuitry of these neurons, we tested whether the AP contributes to a central pathway that innervates the reward center of the brain. Stereotaxic injections of pseudorabies virus were made in the nucleus accumbens (NAc), and after 4 days, this viral tracer produced retrograde transneuronal labeling in the Tryp-OH and non-Tryp-OH AP neurons. Both sets of neurons innervate the NAc via a multisynaptic pathway. Besides sensory information regarding plasma sodium levels, the AP→NAc pathway may also transmit other types of chemosensory information, such as those related to metabolic functions, food intake, and immune system to the subcortical structures of the reward system. Because these subcortical regions ultimately project to the medial prefrontal cortex, different types of chemical signals from visceral systems may influence affective functions.

Reorganization of muscle synergies during multidirectional reaching in the horizontal plane with experimental muscle pain

Muscle pain induces a complex reorganization of the motor strategy which cannot be fully explained by current theories. We tested the hypothesis that the neural control of muscles during reaching in the presence of nociceptive input is determined by a reorganization of muscle synergies with respect to control conditions. Muscle pain was induced by injection of hypertonic saline into the anterior deltoid muscle of eight men. Electromyographic (EMG) signals were recorded from 12 upper limb muscles as subjects performed a reaching task before (baseline) and after the injection of hypertonic (pain) saline, and after the pain sensation vanished. The EMG envelopes were factorized in muscle synergies, and activation signals extracted for each condition. Nociceptive stimulation resulted in a complex muscle reorganization without changes in the kinematic output. The anterior deltoid muscle activity decreased in all subjects while the changes in other muscles were subject specific. Three synergies sufficed to describe the EMG patterns in each condition, suggesting that reaching movements remain modular in the presence of experimental pain. Muscle reorganization in all subjects was accompanied by a change in the activation signals compatible with a change in the central drive to muscles. One, two or three synergies were shared between the baseline and painful conditions, depending on the subject. These results indicate that nociceptive stimulation may induce a reorganization of modular control in reaching. We speculate that such reorganization may be due to the recruitment of synergies specific to the painful condition.

Pain referral and regional deep tissue hyperalgesia in experimental human hip pain models

Hip disorder patients typically present with extensive pain referral and hyperalgesia. To better understand underlying mechanisms, an experimental hip pain model was established in which pain referrals and hyperalgesia could be studied under standardized conditions. In 16 healthy subjects, pain was induced by hypertonic saline injection into the gluteus medius tendon (GMT), adductor longus tendon (ALT), or gluteus medius muscle (GMM). Isotonic saline was injected contralaterally as control. Pain intensity was assessed on a visual analogue scale (VAS), and subjects mapped the pain distribution. Before, during, and after injections, passive hip joint pain provocation tests were completed, together with quantitative sensory testing as follows: pressure pain thresholds (PPTs), cuff algometry pain thresholds (cuff PPTs), cutaneous pin-prick sensitivity, and thermal pain thresholds. Hypertonic saline injected into the GMT resulted in higher VAS scores than hypertonic injections into the ALT and GMM (P<.05). Referred pain areas spread to larger parts of the leg after GMT and GMM injections compared with more regionalized pain pattern after ALT injections (P<.05). PPTs at the injection site were decreased after hypertonic saline injections into GMT and GMM compared with baseline, ALT injections, and isotonic saline. Cuff PPTs from the thigh were decreased after hypertonic saline injections into the ALT compared with baseline, GMT injections, and isotonic saline (P<.05). More subjects had positive joint pain provocation tests after hypertonic compared with isotonic saline injections (P<.05), indicating that this provocation test also assessed hyperalgesia in extra-articular soft tissues. The experimental models may open for better understanding of pain mechanisms associated with painful hip disorders.

Randomised Controlled Trials May Underestimate Drug Effects: Balanced Placebo Trial Design

BackgroundIt is an inherent assumption in randomised controlled trials that the drug effect can be estimated by subtracting the response during placebo from the response during active drug treatment.ObjectiveTo test the assumption of additivity. The primary hypothesis was that the total treatment effect is smaller than the sum of the drug effect and the placebo effect. The secondary hypothesis was that non-additivity was most pronounced in participants with large placebo effects.MethodsWe used a within-subject randomised blinded balanced placebo design and included 48 healthy volunteers (50% males), mean (SD) age 23.4 (6.2) years. Experimental pain was induced by injections of hypertonic saline into the masseter muscle. Participants received four injections with hypertonic saline along with lidocaine or matching placebo in randomised order: A: received hypertonic saline/told hypertonic saline; B: received hypertonic saline+lidocaine/told hypertonic saline; C: received hypertonic saline+placebo/told hypertonic saline+pain killer; D: received hypertonic saline+lidocaine/told hypertonic saline+pain killer. The primary outcome measure was the area under the curve (AUC, mm2) of pain intensity during injections.ResultsThere was a significant difference between the sum of the drug effect and the placebo effect (mean AUC 6279 mm2 (95% CI, 4936–7622)) and the total treatment effect (mean AUC 5455 mm2 (95% CI, 4585–6324)) (P = 0.049). This difference was larger for participants with large versus small placebo effects (P = 0.015), and the difference correlated significantly with the size of the placebo effect (r = 0.65, P = 0.006).ConclusionAlthough this study examined placebo effects and not the whole placebo response as in randomised controlled trials, it does suggest that the additivity assumption may be incorrect, and that the estimated drug effects in randomised controlled trials may be underestimated, particularly in studies reporting large placebo responses. The implications for randomised controlled trials and systematic reviews need to be discussed.

A New Murine Model Of Osmotic Demyelination Syndrome

Event Abstract Back to Event A New Murine Model Of Osmotic Demyelination Syndrome Joanna Bouchat1*, Bruno Couturier2, 3, Fabrice Gankam-Kengné2, 3, Guy Decaux2 and Charles Nicaise1 1 Université de Namur, Laboratory Neurodegeneration and Regeneration, URPhym - NARILIS, Belgium 2 Erasme Hospital, Université Libre de Bruxelles, Research Unit for the Study of Hydromineral Metabolism, Department of General Internal Medicine, Belgium 3 Université Libre de Bruxelles, Laboratory of Histology, Histopathology and Neuroanatomy, Belgium Osmotic demyelination syndrome (ODS) is a severe neurological complication occuring after inadvertant rapid correction of chronic hyponatremia. This pathology primarily affects the CNS and is characterized by large areas of demyelination in centropontine or extrapontine regions, often correlated with clinical symptoms : from lethargia to coma or even death. Historically, the most used ODS animal model is Rattus norvegicus, that mimicked myelin and oligodendrocyte loss and allowed important insights in the management and in the understanding of ODS pathology. According to an adapted protocol from the rat model, we developed a murine model of ODS that will help at unravelling the molecular and cellular pathophysiological mechanisms. Chronic hyponatremia was induced in mice using continuous desmopressin infusion and a low-sodium liquid diet. After 4 days, blood sodium dropped to 113±11 mEq/L in the hyponatremic group (compared to normonatremic group 148±1 mEq/L, p<0.001) and animals showed clinical signs of mild lethargia. Hyponatremia was next corrected by a single injection of hypertonic saline solution targeting a normal range of blood sodium. 24 hours after correction, blood natremia was measured to determine the final 24-hours sodium correction gradient (33±3 mEq/L, p<0.001 between hyponatremia and correction of hyponatremia). Interestingly, mice displayed transient increased overall locomotor activity during the first 12 hours post-correction before a drastic worsening of neurological symptoms, most likely due to occurrence of demyelination. Histopathologically, ODS mice showed large areas of demyelination in subcortical, midbrain regions and in the pons, attested by loss of myelin in Eriochrome R staining and anti-myelin binding protein immunohistochemistry. In conclusion, we successfully translated the rat model of ODS to a mouse model and reproduced the neurological as well as the histological outcomes observed in human cases of ODS. Keywords: Osmotic Demyelination Syndrome, chronic hyponatremia, demyelination, mouse model, histopathological analysis Conference: Belgian Brain Council 2014 MODULATING THE BRAIN: FACTS, FICTION, FUTURE, Ghent, Belgium, 4 Oct - 4 Oct, 2014. Presentation Type: Poster Presentation Topic: Basic Neuroscience Citation: Bouchat J, Couturier B, Gankam-Kengné F, Decaux G and Nicaise C (2014). A New Murine Model Of Osmotic Demyelination Syndrome. Conference Abstract: Belgian Brain Council 2014 MODULATING THE BRAIN: FACTS, FICTION, FUTURE. doi: 10.3389/conf.fnhum.2014.214.00017 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 27 Jun 2014; Published Online: 27 Jun 2014. * Correspondence: Miss. Joanna Bouchat, Université de Namur, Laboratory Neurodegeneration and Regeneration, URPhym - NARILIS, Namur, Belgium, joanna.bouchat@unamur.be Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Joanna Bouchat Bruno Couturier Fabrice Gankam-Kengné Guy Decaux Charles Nicaise Google Joanna Bouchat Bruno Couturier Fabrice Gankam-Kengné Guy Decaux Charles Nicaise Google Scholar Joanna Bouchat Bruno Couturier Fabrice Gankam-Kengné Guy Decaux Charles Nicaise PubMed Joanna Bouchat Bruno Couturier Fabrice Gankam-Kengné Guy Decaux Charles Nicaise Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Resting-state connectivity in the default mode network and insula during experimental low back pain.

Functional magnetic resonance imaging studies have shown that the insular cortex has a significant role in pain identification and information integration, while the default mode network is associated with cognitive and memory-related aspects of pain perception. However, changes in the functional connectivity between the default mode network and insula during pain remain unclear. This study used 3.0 T functional magnetic resonance imaging scans in 12 healthy subjects aged 24.8 ± 3.3 years to compare the differences in the functional activity and connectivity of the insula and default mode network between the baseline and pain condition induced by intramuscular injection of hypertonic saline. Compared with the baseline, the insula was more functionally connected with the medial prefrontal and lateral temporal cortices, whereas there was lower connectivity with the posterior cingulate cortex, precuneus and inferior parietal lobule in the pain condition. In addition, compared with baseline, the anterior cingulate cortex exhibited greater connectivity with the posterior insula, but lower connectivity with the anterior insula, during the pain condition. These data indicate that experimental low back pain led to dysfunction in the connectivity between the insula and default mode network resulting from an impairment of the regions of the brain related to cognition and emotion, suggesting the importance of the interaction between these regions in pain processing.

Intratesticular injection of hypertonic saline : non-invasive alternative method for animal castration model.

Previous studies, including our own, have demonstrated that the intratesticular injection of hypertonic saline (20%) decreased serum testosterone level which was similar to the surgical castration in the rat, showing the state of chemical castration. In the present study, we further verify the efficacy of this less invasive method as an alternative of surgical orchidectomy in the andevrepological field. Sterilized 20% saline was directly injected into the adult male rats (750 μl per testis). The tested rats were divided into 3 groups including intact group (intact), orchidectomy group (ORX) and saline injection group (SAL) after bilateral orchidectomy was performed at the same day of injection. All rats were sacrificed at 4 weeks after injection. The reproductive organs (testes, epididymis, seminal vesicles and prostates) were collected and used for DNA and protein pattern analyses. Also, patho-histological studies on the testes were performed. In contrast to the intact group, similar DNA damages of testis and seminal vesicle were appeared in ORX group and SAL group. The DNA degradations seemed to be the results of necrosis rather than apoptosis. In the protein pattern analysis, all the testing tissues exerted similar patterns in the ORX group and the SAL group compared to the those of intact group. Patho-histological studies revealed that severe degenerative changes in testicular seminiferous tubules and massive infiltration of immune cells in SAL group. The present study confirmed that direct injection of hypertonic saline into the testis caused the equivalent biochemical changes in the accessory sex organs as shown in the orchidectomized animals. These results suggest that hypertonic saline injection model could be a useful castration model which can substitute for surgical castration when its safety is secured through further study in the future.

Influence of Experimental Pain on the Perception of Action Capabilities and Performance of a Maximal Single-Leg Hop

Changes in an individual's state—for example, anxiety/chronic pain—can modify the perception of action capabilities and physical task requirements. In parallel, considerable literature supports altered motor performance during both acute and chronic pain. This study aimed to determine the effect of experimental pain on perception of action capabilities and performance of a dynamic motor task. Performance estimates and actual performance of maximal single-leg hops were recorded for both legs in 13 healthy participants before, during, and after an episode of acute pain induced by a single bolus injection of hypertonic saline into vastus lateralis of 1 leg, with the side counterbalanced among participants. Both estimation of performance and actual performance were smaller (P < .01) during pain than before and after pain. This decrease in estimation and performance during pain was apparent for hops using either leg, but it was greater (P < .01) for the painful leg (−10.8 ± 12.1 cm) than for the control leg (−5.5 ± 7.9 cm). Participants accurately estimated their performance in all conditions for both legs. The results provide evidence that healthy participants have the ability to update the action-scaled relationship between perception and ability during acute pain. PerspectiveThis study demonstrates that the relationship between perceived physical ability and actual performance is effectively updated during acute muscle pain. This match between perceived ability and performance could be relevant during clinical pain assessment, with the potential to be a biomarker of transition from acute to chronic pain state.

Hemodynamic responses elicited by systemic injections of isotonic and hypertonic saline in hemorrhaged rats

PurposeThe objectives of this study were (i) to characterize the hemodynamic responses caused by controlled hemorrhage (HEM) in pentobarbital-anesthetized rats, and (ii) to determine the responses elicited by systemic bolus injections of isotonic saline (0.15M) or hypertonic saline (3M) given 5min after completion of HEM. ResultsControlled HEM (4.3±0.2ml/rat at 1.5ml/min) resulted in a pronounced and sustained fall in mean arterial blood pressure (MAP) to about 40mmHg. The fall in MAP was associated with a reduction in hindquarter vascular resistance (HQR) but no changes in renal (RR) or mesenteric (MR) vascular resistances. Systemic injections of isotonic saline (96–212μmol/kg i.v., in 250–550μl) did not produce immediate responses but promoted the recovery of MAP to levels below pre-HEM values. Systemic injections of hypertonic saline (750–3000μmol/kg, i.v., in 250–550μl) produced immediate and pronounced falls in MAP, RR, MR and especially HQR of 30–120s in duration. However, hypertonic saline prompted a full recovery of MAP, HQR and RR to pre-HEM levels and an increase in MR to levels above pre-HEM values. ConclusionsThis study demonstrates that (i) HEM induced a pronounced fall in MAP which likely involved a fall in cardiac output and HQR, (ii) isotonic saline did not fully normalize MAP, and (iii) hypertonic saline produced dramatic initial responses, and promoted normalization of MAP probably by restoring blood volume and cardiac output through sequestration of fluid from intracellular compartments.