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<meta name="description" content="Search results for: NMDA"> <meta name="keywords" content="NMDA"> <meta name="viewport" content="width=device-width, initial-scale=1, minimum-scale=1, maximum-scale=1, user-scalable=no"> <meta charset="utf-8"> <link href="https://cdn.waset.org/favicon.ico" type="image/x-icon" rel="shortcut icon"> <link href="https://cdn.waset.org/static/plugins/bootstrap-4.2.1/css/bootstrap.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/plugins/fontawesome/css/all.min.css" rel="stylesheet"> <link href="https://cdn.waset.org/static/css/site.css?v=150220211555" rel="stylesheet"> </head> <body> <header> <div class="container"> <nav class="navbar navbar-expand-lg navbar-light"> <a class="navbar-brand" href="https://waset.org"> <img src="https://cdn.waset.org/static/images/wasetc.png" alt="Open Science Research Excellence" title="Open Science Research Excellence" /> </a> <button class="d-block d-lg-none navbar-toggler ml-auto" type="button" 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class="input-group"> <i class="fas fa-search"></i> <input type="text" class="search-query" name="q" placeholder="Author, Title, Abstract, Keywords" value="NMDA"> <input type="submit" class="btn_search" value="Search"> </div> </div> </form> </div> </div> <div class="row mt-3"> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Commenced</strong> in January 2007</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Frequency:</strong> Monthly</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Edition:</strong> International</div> </div> </div> <div class="col-sm-3"> <div class="card"> <div class="card-body"><strong>Paper Count:</strong> 17</div> </div> </div> </div> <h1 class="mt-3 mb-3 text-center" style="font-size:1.6rem;">Search results for: NMDA</h1> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">17</span> Analysis of NMDA Receptor 2B Subunit Gene (GRIN2B) mRNA Expression in the Peripheral Blood Mononuclear Cells of Alzheimer's Disease Patients</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Ali%CC%87%20Bayram">Ali̇ Bayram</a>, <a href="https://publications.waset.org/abstracts/search?q=Semih%20Dalkilic"> Semih Dalkilic</a>, <a href="https://publications.waset.org/abstracts/search?q=Remzi%20Yigiter"> Remzi Yigiter</a> </p> <p class="card-text"><strong>Abstract:</strong></p> N-methyl-D-aspartate (NMDA) receptor is a subtype of glutamate receptor and plays a pivotal role in learning, memory, neuronal plasticity, neurotoxicity and synaptic mechanisms. Animal experiments were suggested that glutamate-induced excitotoxic injuriy and NMDA receptor blockage lead to amnesia and other neurodegenerative diseases including Alzheimer’s disease (AD), Huntington’s disease, amyotrophic lateral sclerosis. Aim of this study is to investigate association between NMDA receptor coding gene GRIN2B expression level and Alzheimer disease. The study was approved by the local ethics committees, and it was conducted according to the principles of the Declaration of Helsinki and guidelines for the Good Clinical Practice. Peripheral blood was collected 50 patients who diagnosed AD and 49 healthy control individuals. Total RNA was isolated with RNeasy midi kit (Qiagen) according to manufacturer’s instructions. After checked RNA quality and quantity with spectrophotometer, GRIN2B expression levels were detected by quantitative real time PCR (QRT-PCR). Statistical analyses were performed, variance between two groups were compared with Mann Whitney U test in GraphpadInstat algorithm with 95 % confidence interval and p < 0.05. After statistical analyses, we have determined that GRIN2B expression levels were down regulated in AD patients group with respect to control group. But expression level of this gene in each group was showed high variability. İn this study, we have determined that NMDA receptor coding gene GRIN2B expression level was down regulated in AD patients when compared with healthy control individuals. According to our results, we have speculated that GRIN2B expression level was associated with AD. But it is necessary to validate these results with bigger sample size. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=Alzheimer%E2%80%99s%20disease" title="Alzheimer’s disease">Alzheimer’s disease</a>, <a href="https://publications.waset.org/abstracts/search?q=N-methyl-d-aspartate%20receptor" title=" N-methyl-d-aspartate receptor"> N-methyl-d-aspartate receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=NR2B" title=" NR2B"> NR2B</a>, <a href="https://publications.waset.org/abstracts/search?q=GRIN2B" title=" GRIN2B"> GRIN2B</a>, <a href="https://publications.waset.org/abstracts/search?q=mRNA%20expression" title=" mRNA expression"> mRNA expression</a>, <a href="https://publications.waset.org/abstracts/search?q=RT-PCR" title=" RT-PCR"> RT-PCR</a> </p> <a href="https://publications.waset.org/abstracts/35375/analysis-of-nmda-receptor-2b-subunit-gene-grin2b-mrna-expression-in-the-peripheral-blood-mononuclear-cells-of-alzheimers-disease-patients" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/35375.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">394</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">16</span> Analysis of Autoantibodies to the S-100 Protein, NMDA, and Dopamine Receptors in Children with Type 1 Diabetes Mellitus</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yuri%20V.%20Bykov">Yuri V. Bykov</a>, <a href="https://publications.waset.org/abstracts/search?q=V.%20%20A.%20Baturin"> V. A. Baturin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aim of the study: The aim of the study was to perform a comparative analysis of the levels of autoantibodies (AAB) to the S-100 protein as well as to the dopamine and NMDA receptors in children with type 1 diabetes mellitus (DM) in therapeutic remission. Materials and methods: Blood serum obtained from 42 children ages 4 to 17 years (20 boys and 22 girls) was analyzed. Twenty-one of these children had a diagnosis of type 1 DM and were in therapeutic remission (study group). The mean duration of disease in children with type 1 DM was 9.6±0.36 years. Children without DM were included in a group of "apparently healthy children" (21 children, comparison group). AAB to the S-100 protein, the dopamine, and NMDA receptors were measured by ELISA. The normal range of IgG AAB was specified as up to 10 µg/mL. In order to compare the central parameters of the groups, the following parametric and non-parametric methods were used: Student's t-test or Mann-Whitney U test. The level of significance for inter-group comparisons was set at p<0.05. Results: The mean levels of AAB to the S-100B protein were significantly higher (p=0.0045) in children with DM (16.84±1.54 µg/mL) when compared with "apparently healthy children" (2.09±0.05 µg/mL). The detected elevated levels of AAB to NMDA receptors may indicate that in children with type 1 DM, there is a change in the activity of the glutamatergic system, which in its turn suggests the presence of excitotoxicity. The mean levels of AAB to dopamine receptors were higher (p=0.0082) in patients comprising the study group than in the children of the comparison group (40.47±2.31 µg/mL and 3.91±0.09 µg/mL). The detected elevated levels of AAB to dopamine receptors suggest an altered activity of the dopaminergic system in children with DM. This can also be viewed as indirect evidence of altered activity of the brain's glutamatergic system. The mean levels of AAB to NMDA receptors were higher in patients with type 1 DM compared with the "apparently healthy children," at 13.16±2.07 µg/mL and 1.304±0.05 µg/mL, respectively (p=0.0021). The elevated mean levels of AAB to the S-100B protein may indicate damage to brain tissue in children with type 1 DM. A difference was also detected between the mean values of the measured AABs, and this difference depended on the duration of the disease: mean AAB values were significantly higher in patients whose disease had lasted more than five years. Conclusions: The elevated mean levels of AAB to the S-100B protein may indicate damage to brain tissue in the setting of excitotoxicity in children with type 1 DM. The discovered elevation of the levels of AAB to NMDA and dopamine receptors may indicate the activation of the glutamatergic and dopaminergic systems. The observed abnormalities indicate the presence of central nervous system damage in children with type 1 DM, with a tendency towards the elevation of the levels of the studied AABs with disease progression. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=autoantibodies" title="autoantibodies">autoantibodies</a>, <a href="https://publications.waset.org/abstracts/search?q=brain%20damage" title=" brain damage"> brain damage</a>, <a href="https://publications.waset.org/abstracts/search?q=children" title=" children"> children</a>, <a href="https://publications.waset.org/abstracts/search?q=diabetes%20mellitus" title=" diabetes mellitus"> diabetes mellitus</a> </p> <a href="https://publications.waset.org/abstracts/154503/analysis-of-autoantibodies-to-the-s-100-protein-nmda-and-dopamine-receptors-in-children-with-type-1-diabetes-mellitus" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/154503.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">96</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">15</span> Differential Expression of Arc in the Mesocorticolimbic System Is Involved in Drug and Natural Rewarding Behavior in Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Yuhua%20Wang">Yuhua Wang</a>, <a href="https://publications.waset.org/abstracts/search?q=Mu%20Li"> Mu Li</a>, <a href="https://publications.waset.org/abstracts/search?q=Jinggen%20Liu"> Jinggen Liu</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Aim: To investigate the different effects of heroin and milk in activating the corticostriatal system that plays a critical role in reward reinforcement learning. Methods: Male SD rats were trained daily for 15 d to self-administer heroin or milk tablets in a classic runway drug self-administration model. Immunohistochemical assay was used to quantify Arc protein expression in the medial prefrontal cortex (mPFC), the nucleus accumbens (NAc), the dorsomedial striatum (DMS) and the ventrolateral striatum (VLS) in response to chronic self-administration of heroin or milk tablets. NMDA receptor antagonist MK801 (0.1 mg/kg) or dopamine D1 receptor antagonist SCH23390 (0.03 mg/kg) were intravenously injected at the same time as heroin was infused intravenously. Results: Runway training with heroin resulted in robust enhancement of Arc expression in the mPFC, the NAc and the DMS on d 1, 7, and 15, and in the VLS on d 1 and d 7. However, runway training with milk led to increased Arc expression in the mPFC, the NAc and the DMS only on d 7 and/or d 15 but not on d 1. Moreover, runway training with milk failed to induce increased Arc protein in the VLS. Both heroin-seeking behavior and Arc protein expression were blocked by MK801 or SCH23390 administration. Conclusion: The VLS is likely to be critically involved in drug-seeking behavior. The NMDA and D1 receptor-dependent Arc expression is important in drug-seeking behavior. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=arc" title="arc">arc</a>, <a href="https://publications.waset.org/abstracts/search?q=mesocorticolimbic%20system" title=" mesocorticolimbic system"> mesocorticolimbic system</a>, <a href="https://publications.waset.org/abstracts/search?q=drug%20rewarding%20behavior" title=" drug rewarding behavior"> drug rewarding behavior</a>, <a href="https://publications.waset.org/abstracts/search?q=NMDA%20receptor" title=" NMDA receptor"> NMDA receptor</a> </p> <a href="https://publications.waset.org/abstracts/2262/differential-expression-of-arc-in-the-mesocorticolimbic-system-is-involved-in-drug-and-natural-rewarding-behavior-in-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/2262.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">391</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">14</span> Investigating the Expression of NR1/NR2 Receptors in Boys Between 6 to 16 with ADHD Compared to a Healthy Controlled Group</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sajad%20Haghshenas">Sajad Haghshenas</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Emerging evidence from clinical, genetic, and animal model studies suggests that the N-methyl-D-aspartate (NMDA) glutamate receptors (NMDAR) may contribute to the pathophysiology and aetiology of neurological and psychiatric disorders and the patients with impaired NMDR receptors experience psychological symptoms. Therefore, we hypothesised that NMDAR receptors play a key role in the development of attention deficit hyperactivity disorder (ADHD). In this comparative analytical study, we utilized western blotting method to assay the expression levels of NMDA subunits NR1 and NR2 in the blood plasma of 50 male individuals diagnosed with ADHD in comparison to 20 healthy controls. The findings from the western blotting analysis provide support for the hypothesis that individuals with ADHD exhibit significantly lower levels of NR1/2 receptors compared to those without the disorder. Further research is needed to explore the potential causal relationship between reduced NR1/NR2 receptor levels and the development of ADHD. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=expression" title="expression">expression</a>, <a href="https://publications.waset.org/abstracts/search?q=glutamate%20receptors" title=" glutamate receptors"> glutamate receptors</a>, <a href="https://publications.waset.org/abstracts/search?q=NR1" title=" NR1"> NR1</a>, <a href="https://publications.waset.org/abstracts/search?q=NR2" title=" NR2"> NR2</a>, <a href="https://publications.waset.org/abstracts/search?q=ADHD" title=" ADHD"> ADHD</a> </p> <a href="https://publications.waset.org/abstracts/170134/investigating-the-expression-of-nr1nr2-receptors-in-boys-between-6-to-16-with-adhd-compared-to-a-healthy-controlled-group" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/170134.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">73</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">13</span> Neuroprotection against N-Methyl-D-Aspartate-Induced Optic Nerve and Retinal Degeneration Changes by Philanthotoxin-343 to Alleviate Visual Impairments Involve Reduced Nitrosative Stress</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Izuddin%20Fahmy%20Abu">Izuddin Fahmy Abu</a>, <a href="https://publications.waset.org/abstracts/search?q=Mohamad%20Haiqal%20Nizar%20Mohamad"> Mohamad Haiqal Nizar Mohamad</a>, <a href="https://publications.waset.org/abstracts/search?q=Muhammad%20Fattah%20Fazel"> Muhammad Fattah Fazel</a>, <a href="https://publications.waset.org/abstracts/search?q=Renu%20Agarwal"> Renu Agarwal</a>, <a href="https://publications.waset.org/abstracts/search?q=Igor%20Iezhitsa"> Igor Iezhitsa</a>, <a href="https://publications.waset.org/abstracts/search?q=Nor%20Salmah%20Bakar"> Nor Salmah Bakar</a>, <a href="https://publications.waset.org/abstracts/search?q=Henrik%20%20Franzyk"> Henrik Franzyk</a>, <a href="https://publications.waset.org/abstracts/search?q=Ian%20Mellor"> Ian Mellor</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Glaucoma is the global leading cause of irreversible blindness. Currently, the available treatment strategy only involves lowering intraocular pressure (IOP); however, the condition often progresses despite lowered or normal IOP in some patients. N-methyl-D-aspartate receptor (NMDAR) excitotoxicity often occurs in neurodegeneration-related glaucoma; thus it is a relevant target to develop a therapy based on neuroprotection approach. This study investigated the effects of Philanthotoxin-343 (PhTX-343), an NMDAR antagonist, on the neuroprotection of NMDA-induced glaucoma to alleviate visual impairments. Male Sprague-Dawley rats were equally divided: Groups 1 (control) and 2 (glaucoma) were intravitreally injected with phosphate buffer saline (PBS) and NMDA (160nM), respectively, while group 3 was pre-treated with PhTX-343 (160nM) 24 hours prior to NMDA injection. Seven days post-treatments, rats were subjected to visual behavior assessments and subsequently euthanized to harvest their retina and optic nerve tissues for histological analysis and determination of nitrosative stress level using 3-nitrotyrosine ELISA. Visual behavior assessments via open field, object, and color recognition tests demonstrated poor visual performance in glaucoma rats indicated by high exploratory behavior. PhTX-343 pre-treatment appeared to preserve visual abilities as all test results were significantly improved (p < 0.05). H&E staining of the retina showed a marked reduction of ganglion cell layer thickness in the glaucoma group; in contrast, PhTX-343 significantly increased the number by 1.28-folds (p < 0.05). PhTX-343 also increased the number of cell nuclei/100μm2 within inner retina by 1.82-folds compared to the glaucoma group (p < 0.05). Toluidine blue staining of optic nerve tissues showed that PhTX-343 reduced the degeneration changes compared to the glaucoma group which exhibited vacuolation overall sections. PhTX-343 also decreased retinal 3- nitrotyrosine concentration by 1.74-folds compared to the glaucoma group (p < 0.05). All results in PhTX-343 group were comparable to control (p > 0.05). We conclude that PhTX-343 protects against NMDA-induced changes and visual impairments in the rat model by reducing nitrosative stress levels. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=excitotoxicity" title="excitotoxicity">excitotoxicity</a>, <a href="https://publications.waset.org/abstracts/search?q=glaucoma" title=" glaucoma"> glaucoma</a>, <a href="https://publications.waset.org/abstracts/search?q=nitrosative%20stress" title=" nitrosative stress "> nitrosative stress </a>, <a href="https://publications.waset.org/abstracts/search?q=NMDA%20receptor" title=" NMDA receptor "> NMDA receptor </a>, <a href="https://publications.waset.org/abstracts/search?q=N-methyl-D-aspartate" title=" N-methyl-D-aspartate "> N-methyl-D-aspartate </a>, <a href="https://publications.waset.org/abstracts/search?q=philanthotoxin" title=" philanthotoxin"> philanthotoxin</a>, <a href="https://publications.waset.org/abstracts/search?q=visual%20behaviour" title=" visual behaviour"> visual behaviour</a> </p> <a href="https://publications.waset.org/abstracts/120388/neuroprotection-against-n-methyl-d-aspartate-induced-optic-nerve-and-retinal-degeneration-changes-by-philanthotoxin-343-to-alleviate-visual-impairments-involve-reduced-nitrosative-stress" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/120388.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">137</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">12</span> Investigation of Possible Behavioural and Molecular Effects of Mobile Phone Exposure on Rats</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=%C3%87.%20G%C3%B6k%C3%A7ek-Sara%C3%A7">Ç. Gökçek-Saraç</a>, <a href="https://publications.waset.org/abstracts/search?q=%C5%9E.%20%C3%96zen"> Ş. Özen</a>, <a href="https://publications.waset.org/abstracts/search?q=N.%20Derin"> N. Derin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The N-methyl-D-aspartate (NMDA)-dependent pathway is the major intracellular signaling pathway implemented in both short- and long-term memory formation in the hippocampus which is the most studied brain structure because of its well documented role in learning and memory. However, little is known about the effects of RF-EMR exposure on NMDA receptor signaling pathway including activation of protein kinases, notably Ca<sup>2+</sup>/calmodulin-dependent protein kinase II alpha (CaMKIIα). The aim of the present study was to investigate the effects of acute and chronic 900 MHz RF-EMR exposure on both passive avoidance behaviour and hippocampal levels of CaMKIIα and its phosphorylated form (pCaMKIIα). Rats were divided into the following groups: Sham rats, and rats exposed to 900 MHz RF-EMR for 2 h/day for 1 week (acute group) or 10 weeks (chronic group), respectively. Passive avoidance task was used as a behavioural method. The hippocampal levels of selected kinases were measured using Western Blotting technique. The results of passive avoidance task showed that both acute and chronic exposure to 900 MHz RF-EMR can impair passive avoidance behaviour with minor effects on chronic group of rats. The analysis of western blot data of selected protein kinases demonstrated that hippocampal levels of CaMKIIα and pCaMKIIα were significantly higher in chronic group of rats as compared to acute groups. Taken together, these findings demonstrated that different duration times (1 week vs 10 weeks) of 900 MHz RF-EMR exposure have different effects on both passive avoidance behaviour of rats and hippocampal levels of selected protein kinases. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=hippocampus" title="hippocampus">hippocampus</a>, <a href="https://publications.waset.org/abstracts/search?q=protein%20kinase" title=" protein kinase"> protein kinase</a>, <a href="https://publications.waset.org/abstracts/search?q=rat" title=" rat"> rat</a>, <a href="https://publications.waset.org/abstracts/search?q=RF-EMR" title=" RF-EMR"> RF-EMR</a> </p> <a href="https://publications.waset.org/abstracts/68567/investigation-of-possible-behavioural-and-molecular-effects-of-mobile-phone-exposure-on-rats" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/68567.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">255</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">11</span> Reduction of Transient Receptor Potential Vanilloid 1 for Chronic Pain and Depression Co-Morbidity through Electroacupuncture and Gene Deletion in Mice Brain</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Bernice%20Lottering">Bernice Lottering</a>, <a href="https://publications.waset.org/abstracts/search?q=Yi-Wen%20Lin"> Yi-Wen Lin</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Chronic pain and depression have an estimated 80% rate of comorbidity with unsatisfactory treatment interventions signifying the importance of developing effective therapeutic interventions for a serious chronic condition affecting a large majority of the global population. Chronic pain is defined as persistent pain presenting for over 3 months. This disease state increases the risk of developing depression in comparison to healthy individuals. In the current study, complete Freund’s adjuvant (CFA) was used to induce cell-mediated chronic inflammatory pain in a murine model. Significant mechanical and thermal hyperalgesia was induced, alongside observable depression-like behaviors. These conditions were attenuated through the use of electroacupuncture (EA). Similarly, these effects were also investigated with respect to the transient receptor potential vanilloid 1 (TRPV1), by analyzing the effects of TRPV1 gene deletion on the comorbidity of chronic pain and depression. The expression of the TRPV1 inflammatory response, and related downstream molecules, including protein kinases (PKs), mitogen-activated protein kinase (MAPKs), and transcriptional factors, were significantly reduced in the thalamus, prefrontal cortex (PFC), hippocampus, and periaqueductal gray (PAG) of CFA-treated mice. In addition, phosphorylated N-methyl-D-aspartate (NMDA) receptor 1 was also found to be reduced in the aforementioned areas, suggesting potential application and validity in a clinical setting. Our study determined the prospective therapeutic effects of EA in the treatment of chronic inflammatory pain and depression comorbidity and provides a novel and detailed mechanism underlying EA-mediated analgesia. These findings may be relevant in the utilization of clinical intervention approaches related to chronic pain and depression comorbidity. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=chronic%20pain" title="chronic pain">chronic pain</a>, <a href="https://publications.waset.org/abstracts/search?q=depression" title=" depression"> depression</a>, <a href="https://publications.waset.org/abstracts/search?q=NMDA" title=" NMDA"> NMDA</a>, <a href="https://publications.waset.org/abstracts/search?q=prefrontal%20cortex" title=" prefrontal cortex"> prefrontal cortex</a>, <a href="https://publications.waset.org/abstracts/search?q=TRPV1" title=" TRPV1"> TRPV1</a> </p> <a href="https://publications.waset.org/abstracts/104336/reduction-of-transient-receptor-potential-vanilloid-1-for-chronic-pain-and-depression-co-morbidity-through-electroacupuncture-and-gene-deletion-in-mice-brain" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/104336.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">133</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">10</span> The Psychosis Prodrome: Biomarkers of the Glutamatergic System and Their Potential Role in Prediction and Treatment</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Peter%20David%20Reiss">Peter David Reiss</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The concept of the psychosis prodrome has allowed for the identification of adolescent and young adult patients who have a significantly elevated risk of developing schizophrenia spectrum disorders. A number of different interventions have been tested in order to prevent or delay progression of symptoms. To date, there has been no consistent meta-analytical evidence to support efficacy of antipsychotic treatment for patients in the prodromal state, and their use remains therefore inconclusive. Although antipsychotics may manage symptoms transiently, they have not been found to prevent or delay onset of psychotic disorders. Furthermore, pharmacological intervention in high-risk individuals remains controversial, because of the antipsychotic side effect profile in a population in which only about 20 to 35 percent will eventually convert to psychosis over a two-year period, with even after two years conversion rates not exceeding 30 to 40 percent. This general estimate is additionally problematic, in that it ignores the fact that there is significant variation in individual risk among clinical high-risk cases. The current lack of reliable tests for at-risk patients makes it difficult to justify individual treatment decisions. Preventive treatment should ideally be dictated by an individual’s risk while minimizing potentially harmful medication exposure. This requires more accurate predictive assessments by using valid and accessible prognostic markers. The following will compare prediction and risk modification potential of behavioral biomarkers such as disturbances of basic sense of self and emotion awareness, neurocognitive biomarkers such as attention, working and declarative memory, and neurophysiological biomarkers such as glutamatergic abnormalities and NMDA receptor dysfunction. Identification of robust biomarkers could therefore not only provide more reliable means of psychosis prediction, but also help test and develop new clinical interventions targeted at the prodromal state. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=at-risk%20mental%20state" title="at-risk mental state">at-risk mental state</a>, <a href="https://publications.waset.org/abstracts/search?q=biomarkers" title=" biomarkers"> biomarkers</a>, <a href="https://publications.waset.org/abstracts/search?q=glutamatergic%20system" title=" glutamatergic system"> glutamatergic system</a>, <a href="https://publications.waset.org/abstracts/search?q=NMDA%20receptor" title=" NMDA receptor"> NMDA receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=psychosis%20prodrome" title=" psychosis prodrome"> psychosis prodrome</a>, <a href="https://publications.waset.org/abstracts/search?q=schizophrenia" title=" schizophrenia"> schizophrenia</a> </p> <a href="https://publications.waset.org/abstracts/75698/the-psychosis-prodrome-biomarkers-of-the-glutamatergic-system-and-their-potential-role-in-prediction-and-treatment" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/75698.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">195</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">9</span> Oleic Acid Enhances Hippocampal Synaptic Efficacy</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Rema%20Vazhappilly">Rema Vazhappilly</a>, <a href="https://publications.waset.org/abstracts/search?q=Tapas%20Das"> Tapas Das </a> </p> <p class="card-text"><strong>Abstract:</strong></p> Oleic acid is a cis unsaturated fatty acid and is known to be a partially essential fatty acid due to its limited endogenous synthesis during pregnancy and lactation. Previous studies have demonstrated the role of oleic acid in neuronal differentiation and brain phospholipid synthesis. These evidences indicate a major role for oleic acid in learning and memory. Interestingly, oleic acid has been shown to enhance hippocampal long term potentiation (LTP), the physiological correlate of long term synaptic plasticity. However the effect of oleic acid on short term synaptic plasticity has not been investigated. Short term potentiation (STP) is the physiological correlate of short term synaptic plasticity which is the key underlying molecular mechanism of short term memory and neuronal information processing. STP in the hippocampal CA1 region has been known to require the activation of N-methyl-D-aspartate receptors (NMDARs). The NMDAR dependent hippocampal STP as a potential mechanism for short term memory has been a subject of intense interest for the past few years. Therefore in the present study the effect of oleic acid on NMDAR dependent hippocampal STP was determined in mouse hippocampal slices (in vitro) using Multi-electrode array system. STP was induced by weak tetanic Stimulation (one train of 100 Hz stimulations for 0.1s) of the Schaffer collaterals of CA1 region of the hippocampus in slices treated with different concentrations of oleic acid in presence or absence of NMDAR antagonist D-AP5 (30 µM) . Oleic acid at 20 (mean increase in fEPSP amplitude = ~135 % Vs. Control = 100%; P<0.001) and 30 µM (mean increase in fEPSP amplitude = ~ 280% Vs. Control = 100%); P<0.001) significantly enhanced the STP following weak tetanic stimulation. Lower oleic acid concentrations at 10 µM did not modify the hippocampal STP induced by weak tetanic stimulation. The hippocampal STP induced by weak tetanic stimulation was completely blocked by the NMDA receptor antagonist D-AP5 (30µM) in both oleic acid and control treated hippocampal slices. This lead to the conclusion that the hippocampal STP elicited by weak tetanic stimulation and enhanced by oleic acid was NMDAR dependent. Together these findings suggest that oleic acid may enhance the short term memory and neuronal information processing through the modulation of NMDAR dependent hippocampal short-term synaptic plasticity. In conclusion this study suggests the possible role of oleic acid to prevent the short term memory loss and impaired neuronal function throughout development. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=oleic%20acid" title="oleic acid">oleic acid</a>, <a href="https://publications.waset.org/abstracts/search?q=short-term%20potentiation" title=" short-term potentiation"> short-term potentiation</a>, <a href="https://publications.waset.org/abstracts/search?q=memory" title=" memory"> memory</a>, <a href="https://publications.waset.org/abstracts/search?q=field%20excitatory%20post%20synaptic%20potentials" title=" field excitatory post synaptic potentials"> field excitatory post synaptic potentials</a>, <a href="https://publications.waset.org/abstracts/search?q=NMDA%20receptor" title=" NMDA receptor"> NMDA receptor</a> </p> <a href="https://publications.waset.org/abstracts/36993/oleic-acid-enhances-hippocampal-synaptic-efficacy" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/36993.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">335</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">8</span> The 5-HT1A Receptor Biased Agonists, NLX-101 and NLX-204, Elicit Rapid-Acting Antidepressant Activity in Rat Similar to Ketamine and via GABAergic Mechanisms</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=A.%20Newman-Tancredi">A. Newman-Tancredi</a>, <a href="https://publications.waset.org/abstracts/search?q=R.%20Depoort%C3%A8re"> R. Depoortère</a>, <a href="https://publications.waset.org/abstracts/search?q=P.%20Gruca"> P. Gruca</a>, <a href="https://publications.waset.org/abstracts/search?q=E.%20Litwa"> E. Litwa</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20Lason"> M. Lason</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20Papp"> M. Papp</a> </p> <p class="card-text"><strong>Abstract:</strong></p> The N-methyl-D-aspartic acid (NMDA) receptor antagonist, ketamine, can elicit rapid-acting antidepressant (RAAD) effects in treatment-resistant patients, but it requires parenteral co-administration with a classical antidepressant under medical supervision. In addition, ketamine can also produce serious side effects that limit its long-term use, and there is much interest in identifying RAADs based on ketamine’s mechanism of action but with safer profiles. Ketamine elicits GABAergic interneuron inhibition, glutamatergic neuron stimulation, and, notably, activation of serotonin 5-HT1A receptors in the prefrontal cortex (PFC). Direct activation of the latter receptor subpopulation with selective ‘biased agonists’ may therefore be a promising strategy to identify novel RAADs and, consistent with this hypothesis, the prototypical cortical biased agonist, NLX-101, exhibited robust RAAD-like activity in the chronic mild stress model of depression (CMS). The present study compared the effects of a novel, selective 5-HT1A receptor-biased agonist, NLX-204, with those of ketamine and NLX-101. Materials and methods: CMS procedure was conducted on Wistar rats; drugs were administered either intraperitoneally (i.p.) or by bilateral intracortical microinjection. Ketamine: 10 mg/kg i.p. or 10 µg/side in PFC; NLX-204 and NLX-101: 0.08 and 0.16 mg/kg i.p. or 16 µg/side in PFC. In addition, interaction studies were carried out with systemic NLX-204 or NLX-101 (each at 0.16 mg/kg i.p.) in combination with intracortical WAY-100635 (selective 5-HT1A receptor antagonist; 2 µg/side) or muscimol (GABA-A receptor agonist, 12.5 ng/side). Anhedonia was assessed by CMS-induced decrease in sucrose solution consumption; anxiety-like behavior was assessed using the Elevated Plus Maze (EPM), and cognitive impairment was assessed by the Novel Object Recognition (NOR) test. Results: A single administration of NLX-204 was sufficient to reverse the CMS-induced deficit in sucrose consumption, similarly to ketamine and NLX-101. NLX-204 also reduced CMS-induced anxiety in the EPM and abolished CMS-induced NOR deficits. These effects were maintained (EPM and NOR) or enhanced (sucrose consumption) over a subsequent 2-week period of treatment. The anti-anhedonic response of the drugs was also maintained for several weeks Following treatment discontinuation, suggesting that they had sustained effects on neuronal networks. A single PFC administration of NLX-204 reversed deficient sucrose consumption, similarly to ketamine and NLX-101. Moreover, the anti-anhedonic activities of systemic NLX-204 and NLX 101 were abolished by coadministration with intracortical WAY-100635 or muscimol. Conclusions: (i) The antidepressant-like activity of NLX-204 in the rat CMS model was as rapid as that of ketamine or NLX-101, supporting targeting cortical 5-HT1A receptors with selective, biased agonists to achieve RAAD effects. (ii)The anti-anhedonic activity of systemic NLX-204 was mimicked by local administration of the compound in the PFC, confirming the involvement of cortical circuits in its RAAD-like effects. (iii) Notably, the effects of systemic NLX-204 and NLX-101 were abolished by PFC administration of muscimol, indicating that they act by (indirectly) eliciting a reduction in cortical GABAergic neurotransmission. This is consistent with ketamine’s mechanism of action and suggests that there are converging NMDA and 5-HT1A receptor signaling cascades in PFC underlying the RAAD-like activities of ketamine and NLX-204. Acknowledgements: The study was financially supported by NCN grant no. 2019/35/B/NZ7/00787. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=depression" title="depression">depression</a>, <a href="https://publications.waset.org/abstracts/search?q=ketamine" title=" ketamine"> ketamine</a>, <a href="https://publications.waset.org/abstracts/search?q=serotonin" title=" serotonin"> serotonin</a>, <a href="https://publications.waset.org/abstracts/search?q=5-HT1A%20receptor" title=" 5-HT1A receptor"> 5-HT1A receptor</a>, <a href="https://publications.waset.org/abstracts/search?q=chronic%20mild%20stress" title=" chronic mild stress"> chronic mild stress</a> </p> <a href="https://publications.waset.org/abstracts/153699/the-5-ht1a-receptor-biased-agonists-nlx-101-and-nlx-204-elicit-rapid-acting-antidepressant-activity-in-rat-similar-to-ketamine-and-via-gabaergic-mechanisms" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/153699.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">113</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">7</span> Targeting Calcium Dysregulation for Treatment of Dementia in Alzheimer's Disease</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Huafeng%20Wei">Huafeng Wei</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Dementia in Alzheimer’s Disease (AD) is the number one cause of dementia internationally, without effective treatments. Increasing evidence suggest that disruption of intracellular calcium homeostasis, primarily pathological elevation of cytosol and mitochondria but reduction of endoplasmic reticulum (ER) calcium concentrations, play critical upstream roles on multiple pathologies and associated neurodegeneration, impaired neurogenesis, synapse, and cognitive dysfunction in various AD preclinical studies. The last federal drug agency (FDA) approved drug for AD dementia treatment, memantine, exert its therapeutic effects by ameliorating N-methyl-D-aspartate (NMDA) glutamate receptor overactivation and subsequent calcium dysregulation. More research works are needed to develop other drugs targeting calcium dysregulation at multiple pharmacological acting sites for future effective AD dementia treatment. Particularly, calcium channel blockers for the treatment of hypertension and dantrolene for the treatment of muscle spasm and malignant hyperthermia can be repurposed for this purpose. In our own research work, intranasal administration of dantrolene significantly increased its brain concentrations and durations, rendering it a more effective therapeutic drug with less side effects for chronic AD dementia treatment. This review summarizesthe progress of various studies repurposing drugs targeting calcium dysregulation for future effective AD dementia treatment as potentially disease-modifying drugs. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=alzheimer" title="alzheimer">alzheimer</a>, <a href="https://publications.waset.org/abstracts/search?q=calcium" title=" calcium"> calcium</a>, <a href="https://publications.waset.org/abstracts/search?q=cognitive%20dysfunction" title=" cognitive dysfunction"> cognitive dysfunction</a>, <a href="https://publications.waset.org/abstracts/search?q=dementia" title=" dementia"> dementia</a>, <a href="https://publications.waset.org/abstracts/search?q=neurodegeneration" title=" neurodegeneration"> neurodegeneration</a>, <a href="https://publications.waset.org/abstracts/search?q=neurogenesis" title=" neurogenesis"> neurogenesis</a> </p> <a href="https://publications.waset.org/abstracts/136963/targeting-calcium-dysregulation-for-treatment-of-dementia-in-alzheimers-disease" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/136963.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">182</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">6</span> Factors Associated with Ketamine Use in Pancreatic Cancer Patient in a Single Hospice Center</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Kyung%20Min%20Kwom">Kyung Min Kwom</a>, <a href="https://publications.waset.org/abstracts/search?q=Young%20Joo%20Lee"> Young Joo Lee</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Purpose: Up to 90% of pancreatic cancer patient suffer from neuropathic pain. In palliative care setting, pain control in a pancreatic cancer patient is one of the major goals. Ketamine is a NMDA receptor antagonist effective in neuropathic pain. Also, there have been studies about opioid sparing effect of ketamine. This study was held in palliative care unit among pancreatic cancer patients to find out the factors related to ketamine use and the opioid sparing effect. Methods: Medical records of pancreatic cancer patients admitted to St. Mary’s hospital palliative care unit from 2013.1 to 2014.12 were reviewed. Patients were divided into two categories according to ketamine use. Also, opioid use before and after ketamine use was compared in ketamine group. Results: Compared to non ketamine use group, patients in ketamine group required a higher dose of opioid. Total opioid dose, daily opioid dose, number of daily rescue medication, daily average rescue dose were statistically significantly higher in ketamine group. Opioid requirement was increased after ketamine administration. Conclusion: In this study, ketamine group required more opioid. Ketamine is frequently considered in patients with severe pain, requiring high amount of opioid. Also, ketamine did not have an opioid sparing effect. Future studies about palliative use of ketamine in a larger number of patients are required. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=ketamine" title="ketamine">ketamine</a>, <a href="https://publications.waset.org/abstracts/search?q=opioid%20sparing" title=" opioid sparing"> opioid sparing</a>, <a href="https://publications.waset.org/abstracts/search?q=palliative%20care" title=" palliative care"> palliative care</a>, <a href="https://publications.waset.org/abstracts/search?q=pancreatic%20cancer" title=" pancreatic cancer"> pancreatic cancer</a> </p> <a href="https://publications.waset.org/abstracts/54663/factors-associated-with-ketamine-use-in-pancreatic-cancer-patient-in-a-single-hospice-center" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/54663.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">234</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">5</span> Clinical Comparative Study Comparing Efficacy of Intrathecal Fentanyl and Magnesium as an Adjuvant to Hyperbaric Bupivacaine in Mild Pre-Eclamptic Patients Undergoing Caesarean Section</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Sanchita%20B.%20Sarma">Sanchita B. Sarma</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20P.%20Nath"> M. P. Nath</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Adequate analgesia following caesarean section decreases morbidity, hastens ambulation, improves patient outcome and facilitates care of the newborn. Intrathecal magnesium, an NMDA antagonist, has been shown to prolong analgesia without significant side effects in healthy parturients. The aim of this study was to evaluate the onset and duration of sensory and motor block, hemodynamic effect, postoperative analgesia, and adverse effects of magnesium or fentanyl given intrathecally with hyperbaric 0.5% bupivacaine in patients with mild preeclampsia undergoing caesarean section. Sixty women with mild preeclampsia undergoing elective caesarean section were included in a prospective, double blind, controlled trial. Patients were randomly assigned to receive spinal anesthesia with 2 mL 0.5% hyperbaric bupivacaine with 12.5 µg fentanyl (group F) or 0.1 ml of 50% magnesium sulphate (50 mg) (group M) with 0.15ml preservative free distilled water. Onset, duration and recovery of sensory and motor block, time to maximum sensory block, duration of spinal anaesthesia and postoperative analgesic requirements were studied. Statistical comparison was carried out using the Chi-square or Fisher’s exact tests and Independent Student’s t-test where appropriate. The onset of both sensory and motor block was slower in the magnesium group. The duration of spinal anaesthesia (246 vs. 284) and motor block (186.3 vs. 210) were significantly longer in the magnesium group. Total analgesic top up requirement was less in group M. Hemodynamic parameters were similar in both the groups. Intrathecal magnesium caused minimal side effects. Since Fentanyl and other opioid congeners are not available throughout the country easily, magnesium with its easy availability and less side effect profile can be a cost effective alternative to fentanyl in managing pregnancy induced hypertension (PIH) patients given along with Bupivacaine intrathecally in caesarean section. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=analgesia" title="analgesia">analgesia</a>, <a href="https://publications.waset.org/abstracts/search?q=magnesium" title=" magnesium"> magnesium</a>, <a href="https://publications.waset.org/abstracts/search?q=pre%20eclampsia" title=" pre eclampsia"> pre eclampsia</a>, <a href="https://publications.waset.org/abstracts/search?q=spinal%20anaesthesia" title=" spinal anaesthesia"> spinal anaesthesia</a> </p> <a href="https://publications.waset.org/abstracts/29667/clinical-comparative-study-comparing-efficacy-of-intrathecal-fentanyl-and-magnesium-as-an-adjuvant-to-hyperbaric-bupivacaine-in-mild-pre-eclamptic-patients-undergoing-caesarean-section" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/29667.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">321</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">4</span> Differentiation of Drug Stereoisomers by Their Stereostructure-Selective Membrane Interactions as One of Pharmacological Mechanisms</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Maki%20Mizogami">Maki Mizogami</a>, <a href="https://publications.waset.org/abstracts/search?q=Hironori%20Tsuchiya"> Hironori Tsuchiya</a>, <a href="https://publications.waset.org/abstracts/search?q=Yoshiroh%20Hayabuchi"> Yoshiroh Hayabuchi</a>, <a href="https://publications.waset.org/abstracts/search?q=Kenji%20Shigemi"> Kenji Shigemi</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Since drugs exhibit significant structure-dependent differences in activity and toxicity, their differentiation based on the mechanism of action should have implications for comparative drug efficacy and safety. We aimed to differentiate drug stereoisomers by their stereostructure-selective membrane interactions underlying pharmacological and toxicological effects. Biomimetic lipid bilayer membranes were prepared with phospholipids and sterols (either cholesterol or epicholesterol) to mimic the lipid compositions of neuronal and cardiomyocyte membranes and to provide these membranes with the chirality. The membrane preparations were treated with different classes of stereoisomers at clinically- and pharmacologically-relevant concentrations (25-200 μM), followed by measuring fluorescence polarization to determine the membrane interactivity of drugs to change the physicochemical property of membranes. All the tested drugs acted on lipid bilayers to increase or decrease the membrane fluidity. Drug stereoisomers could not be differentiated when interacting with the membranes consisting of phospholipids alone. However, they stereostructure-selectively interacted with neuro-mimetic and cardio-mimetic membranes containing 40 mol% cholesterol ((3β)-cholest-5-en-3-ol) to show the relative potencies being local anesthetic R(+)-bupivacaine > rac-bupivacaine > S(‒)-bupivacaine, α2-adrenergic agonistic D-medetomidine > rac-medetomidine > L-medetomidine, β-adrenergic antagonistic R(+)-propranolol > rac-propranolol > S(–)-propranolol, NMDA receptor antagonistic S(+)-ketamine > rac-ketamine, analgesic monoterpenoid (+)-menthol > (‒)-menthol, non-steroidal anti-inflammatory S(+)-ibuprofen > rac-ibuprofen > R(‒)-ibuprofen, and bioactive flavonoid (+)-epicatechin > (‒)-epicatechin. All of the order of membrane interactivity were correlated to those of beneficial and adverse effects of the tested stereoisomers. In contrast, the membranes prepared with epicholesterol ((3α)-chotest-5-en-3-ol), an epimeric form of cholesterol, reversed the rank order of membrane interactivity to be S(‒)-enantiomeric > racemic > R(+)-enantiomeric bupivacaine, L-enantiomeric > racemic > D-enantiomeric medetomidine, S(–)-enantiomeric > racemic > R(+)-enantiomeric propranolol, racemic > S(+)-enantiomeric ketamine, (‒)-enantiomeric > (+)-enantiomeric menthol, R(‒)-enantiomeric > racemic > S(+)-enantiomeric ibuprofen, and (‒)-enantiomeric > (+)-enantiomeric epicatechin. The opposite configuration allows drug molecules to interact with chiral sterol membranes enantiomer-selectively. From the comparative results, it is speculated that a 3β-hydroxyl group in cholesterol is responsible for the enantioselective interactions of drugs. In conclusion, the differentiation of drug stereoisomers by their stereostructure-selective membrane interactions would be useful for designing and predicting drugs with higher activity and/or lower toxicity. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=chiral%20membrane" title="chiral membrane">chiral membrane</a>, <a href="https://publications.waset.org/abstracts/search?q=differentiation" title=" differentiation"> differentiation</a>, <a href="https://publications.waset.org/abstracts/search?q=drug%20stereoisomer" title=" drug stereoisomer"> drug stereoisomer</a>, <a href="https://publications.waset.org/abstracts/search?q=enantioselective%20membrane%20interaction" title=" enantioselective membrane interaction"> enantioselective membrane interaction</a> </p> <a href="https://publications.waset.org/abstracts/57851/differentiation-of-drug-stereoisomers-by-their-stereostructure-selective-membrane-interactions-as-one-of-pharmacological-mechanisms" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/57851.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">223</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">3</span> Is Brain Death Reversal Possible in Near Future: Intrathecal Sodium Nitroprusside (SNP) Superfusion in Brain Death Patients=The 10,000 Fold Effect</h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Vinod%20Kumar%20Tewari">Vinod Kumar Tewari</a>, <a href="https://publications.waset.org/abstracts/search?q=Mazhar%20Husain"> Mazhar Husain</a>, <a href="https://publications.waset.org/abstracts/search?q=Hari%20Kishan%20Das%20Gupta"> Hari Kishan Das Gupta</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Primary or secondary brain death is also accompanied with vasospasm of the perforators other than tissue disruption & further exaggerates the anoxic damage, in the form of neuropraxia. In normal conditions the excitatory impulse propagates as anterograde neurotransmission (ANT) and at the level of synapse, glutamate activates NMDA receptors on postsynaptic membrane. Nitric oxide (NO) is produced by Nitric oxide Synthetase (NOS) in postsynaptic dendride or cell body and travels backwards across a chemical synapse to bind to the axon terminal of a presynaptic neuron for regulation of ANT this process is called as the retrograde neurotransmission (RNT). Thus the primary function of NO is RNT and the purpose of RNT is regulation of chemical neurotransmission at synapse. For this reason, RNT allows neural circuits to create feedback loops. The haem is the ligand binding site of NO receptor (sGC) at presynaptic membrane. The affinity of haem exhibits > 10,000-fold excess for NO than Oxygen (THE 10,000 FOLD EFFECT). In pathological conditions ANT, normal synaptic activity including RNT is absent. NO donors like sodium nitroprusside (SNP) releases NO by activating NOS at the level of postsynaptic area. NO now travels backwards across a chemical synapse to bind to the haem of NO receptor at axon terminal of a presynaptic neuron as in normal condition. NO now acts as impulse generator (at presynaptic membrane) thus bypasses the normal ANT. Also the arteriolar perforators are having Nitric Oxide Synthetase (NOS) at the adventitial side (outer border) on which sodium nitroprusside (SNP) acts; causing release of Nitric Oxide (NO) which vasodilates the perforators causing gush of blood in brain’s tissue and reversal of brain death. Objective: In brain death cases we only think for various transplantations but this study being a pilot study reverses some criteria of brain death by vasodilating the arteriolar perforators. To study the effect of intrathecal sodium nitroprusside (IT SNP) in cases of brain death in which: 1. Retrograde transmission = assessed by the hyperacute timings of reversal 2. The arteriolar perforator vasodilatation caused by NO and the maintenance of reversal of brain death reversal. Methods: 35 year old male, who became brain death after head injury and has not shown any signs of improvement after every maneuver for 6 hours, a single superfusion done by SNP via transoptic canal route for quadrigeminal cistern and cisternal puncture for IV ventricular with SNP done. Results: He showed spontaneous respiration (7 bouts) with TCD studies showing start of pulsations of various branches of common carotid arteries. Conclusions: In future we can give this SNP via transoptic canal route and in IV ventricle before declaring the body to be utilized for transplantations or dead or in broader way we can say that in near future it is possible to revert back from brain death or we have to modify our criterion. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=brain%20death" title="brain death">brain death</a>, <a href="https://publications.waset.org/abstracts/search?q=intrathecal%20sodium%20nitroprusside" title=" intrathecal sodium nitroprusside"> intrathecal sodium nitroprusside</a>, <a href="https://publications.waset.org/abstracts/search?q=TCD%20studies" title=" TCD studies"> TCD studies</a>, <a href="https://publications.waset.org/abstracts/search?q=perforators" title=" perforators"> perforators</a>, <a href="https://publications.waset.org/abstracts/search?q=vasodilatations" title=" vasodilatations"> vasodilatations</a>, <a href="https://publications.waset.org/abstracts/search?q=retrograde%20transmission" title=" retrograde transmission"> retrograde transmission</a>, <a href="https://publications.waset.org/abstracts/search?q=10" title=" 10"> 10</a>, <a href="https://publications.waset.org/abstracts/search?q=000%20fold%20effect" title="000 fold effect">000 fold effect</a> </p> <a href="https://publications.waset.org/abstracts/13410/is-brain-death-reversal-possible-in-near-future-intrathecal-sodium-nitroprusside-snp-superfusion-in-brain-death-patientsthe-10000-fold-effect" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/13410.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">403</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">2</span> The 10,000 Fold Effect of Retrograde Neurotransmission, a New Concept for Stroke Revival: Use of Intracarotid Sodium Nitroprusside </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=Vinod%20Kumar">Vinod Kumar</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Tissue Plasminogen Activator (tPA) showed a level 1 benefit in acute stroke (within 3-6 hrs). Intracarotid sodium nitroprusside (ICSNP) has been studied in this context with a wide treatment window, fast recovery and affordability. This work proposes two mechanisms for acute cases and one mechanism for chronic cases, which are interrelated, for physiological recovery. a)Retrograde Neurotransmission (acute cases): 1)Normal excitatory impulse: at the synaptic level, glutamate activates NMDA receptors, with nitric oxide synthetase (NOS) on the postsynaptic membrane, for further propagation by the calcium-calmodulin complex. Nitric oxide (NO, produced by NOS) travels backward across the chemical synapse and binds the axon-terminal NO receptor/sGC of a presynaptic neuron, regulating anterograde neurotransmission (ANT) via retrograde neurotransmission (RNT). Heme is the ligand-binding site of the NO receptor/sGC. Heme exhibits > 10,000-fold higher affinity for NO than for oxygen (the 10,000-fold effect) and is completed in 20 msec. 2)Pathological conditions: normal synaptic activity, including both ANT and RNT, is absent. A NO donor (SNP) releases NO from NOS in the postsynaptic region. NO travels backward across a chemical synapse to bind to the heme of a NO receptor in the axon terminal of a presynaptic neuron, generating an impulse, as under normal conditions. b)Vasospasm: (acute cases) Perforators show vasospastic activity. NO vasodilates the perforators via the NO-cAMP pathway. c)Long-Term Potentıatıon (LTP): (chronic cases) The NO–cGMP-pathway plays a role in LTP at many synapses throughout the CNS and at the neuromuscular junction. LTP has been reviewed both generally and with respect to brain regions specific for memory/learning. Aims/Study Des’gn: The principles of “generation of impulses from the presynaptic region to the postsynaptic region by very potent RNT (10,000-fold effect)” and “vasodilation of arteriolar perforators” are the basis of the authors’ hypothesis to treat stroke cases. Case-control prospective study. Mater’als And Methods: The experimental population included 82 stroke patients (10 patients were given control treatments without superfusion or with 5% dextrose superfusion, and 72 patients comprised the ICSNP group). The mean time for superfusion was 9.5 days post-stroke. Pre- and post-ICSNP status was monitored by NIHSS, MRI and TCD. Results: After 90 seconds in the ICSNP group, the mean change in the NIHSS score was a decrease of 1.44 points, or 6.55%; after 2 h, there was a decrease of 1.16 points; after 24 h, there was an increase of 0.66 points, 2.25%, compared to the control-group increase of 0.7 points, or 3.53%; at 7 days, there was an 8.61-point decrease, 44.58%, compared to the control-group increase of 2.55 points, or 22.37%; at 2 months in ICSNP, there was a 6.94-points decrease, 62.80%, compared to the control-group decrease of 2.77 points, or 8.78%. TCD was documented and improvements were noted. Conclusions: ICSNP is a swift-acting drug in the treatment of stroke, acting within 90 seconds on day 9.5 post-stroke with a small decrease after 24 hours. The drug recovers from this decrease quickly. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=brain%20infarcts" title="brain infarcts">brain infarcts</a>, <a href="https://publications.waset.org/abstracts/search?q=intracarotid%20sodium%20nitroprusside" title=" intracarotid sodium nitroprusside"> intracarotid sodium nitroprusside</a>, <a href="https://publications.waset.org/abstracts/search?q=perforators" title=" perforators"> perforators</a>, <a href="https://publications.waset.org/abstracts/search?q=vasodilat%C4%B1ons" title=" vasodilatıons"> vasodilatıons</a>, <a href="https://publications.waset.org/abstracts/search?q=retrograde%20transmission" title=" retrograde transmission"> retrograde transmission</a>, <a href="https://publications.waset.org/abstracts/search?q=the%2010" title=" the 10"> the 10</a>, <a href="https://publications.waset.org/abstracts/search?q=000-fold%20effect" title="000-fold effect">000-fold effect</a> </p> <a href="https://publications.waset.org/abstracts/15756/the-10000-fold-effect-of-retrograde-neurotransmission-a-new-concept-for-stroke-revival-use-of-intracarotid-sodium-nitroprusside" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/15756.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">309</span> </span> </div> </div> <div class="card paper-listing mb-3 mt-3"> <h5 class="card-header" style="font-size:.9rem"><span class="badge badge-info">1</span> The 10,000 Fold Effect of Retrograde Neurotransmission: A New Concept for Cerebral Palsy Revival by the Use of Nitric Oxide Donars </h5> <div class="card-body"> <p class="card-text"><strong>Authors:</strong> <a href="https://publications.waset.org/abstracts/search?q=V.%20K.%20Tewari">V. K. Tewari</a>, <a href="https://publications.waset.org/abstracts/search?q=M.%20Hussain"> M. Hussain</a>, <a href="https://publications.waset.org/abstracts/search?q=H.%20K.%20D.%20Gupta"> H. K. D. Gupta</a> </p> <p class="card-text"><strong>Abstract:</strong></p> Background: Nitric Oxide Donars (NODs) (intrathecal sodium nitroprusside (ITSNP) and oral tadalafil 20mg post ITSNP) has been studied in this context in cerebral palsy patients for fast recovery. This work proposes two mechanisms for acute cases and one mechanism for chronic cases, which are interrelated, for physiological recovery. a) Retrograde Neurotransmission (acute cases): 1) Normal excitatory impulse: at the synaptic level, glutamate activates NMDA receptors, with nitric oxide synthetase (NOS) on the postsynaptic membrane, for further propagation by the calcium-calmodulin complex. Nitric oxide (NO, produced by NOS) travels backward across the chemical synapse and binds the axon-terminal NO receptor/sGC of a presynaptic neuron, regulating anterograde neurotransmission (ANT) via retrograde neurotransmission (RNT). Heme is the ligand-binding site of the NO receptor/sGC. Heme exhibits > 10,000-fold higher affinity for NO than for oxygen (the 10,000-fold effect) and is completed in 20 msec. 2) Pathological conditions: normal synaptic activity, including both ANT and RNT, is absent. A NO donor (SNP) releases NO from NOS in the postsynaptic region. NO travels backward across a chemical synapse to bind to the heme of a NO receptor in the axon terminal of a presynaptic neuron, generating an impulse, as under normal conditions. b) Vasopasm: (acute cases) Perforators show vasospastic activity. NO vasodilates the perforators via the NO-cAMP pathway. c) Long-Term Potentiation (LTP): (chronic cases) The NO–cGMP-pathway plays a role in LTP at many synapses throughout the CNS and at the neuromuscular junction. LTP has been reviewed both generally and with respect to brain regions specific for memory/learning. Aims/Study Design: The principles of “generation of impulses from the presynaptic region to the postsynaptic region by very potent RNT (10,000-fold effect)” and “vasodilation of arteriolar perforators” are the basis of the authors’ hypothesis to treat cerebral palsy cases. Case-control prospective study. Materials and Methods: The experimental population included 82 cerebral palsy patients (10 patients were given control treatments without NOD or with 5% dextrose superfusion, and 72 patients comprised the NOD group). The mean time for superfusion was 5 months post-cerebral palsy. Pre- and post-NOD status was monitored by Gross Motor Function Classification System for Cerebral Palsy (GMFCS), MRI, and TCD studies. Results: After 7 days in the NOD group, the mean change in the GMFCS score was an increase of 1.2 points mean; after 3 months, there was an increase of 3.4 points mean, compared to the control-group increase of 0.1 points at 3 months. MRI and TCD documented the improvements. Conclusions: NOD (ITSNP boosts up the recovery and oral tadalafil maintains the recovery to a well-desired level) acts swiftly in the treatment of CP, acting within 7 days on 5 months post-cerebral palsy either of the three mechanisms. <p class="card-text"><strong>Keywords:</strong> <a href="https://publications.waset.org/abstracts/search?q=cerebral%20palsy" title="cerebral palsy">cerebral palsy</a>, <a href="https://publications.waset.org/abstracts/search?q=intrathecal%20sodium%20nitroprusside" title=" intrathecal sodium nitroprusside"> intrathecal sodium nitroprusside</a>, <a href="https://publications.waset.org/abstracts/search?q=oral%20tadalafil" title=" oral tadalafil"> oral tadalafil</a>, <a href="https://publications.waset.org/abstracts/search?q=perforators" title=" perforators"> perforators</a>, <a href="https://publications.waset.org/abstracts/search?q=vasodilations" title=" vasodilations"> vasodilations</a>, <a href="https://publications.waset.org/abstracts/search?q=retrograde%20transmission" title=" retrograde transmission"> retrograde transmission</a>, <a href="https://publications.waset.org/abstracts/search?q=the%2010" title=" the 10"> the 10</a>, <a href="https://publications.waset.org/abstracts/search?q=000-fold%20effect" title="000-fold effect">000-fold effect</a>, <a href="https://publications.waset.org/abstracts/search?q=long-term%20potantiation" title=" long-term potantiation"> long-term potantiation</a> </p> <a href="https://publications.waset.org/abstracts/15995/the-10000-fold-effect-of-retrograde-neurotransmission-a-new-concept-for-cerebral-palsy-revival-by-the-use-of-nitric-oxide-donars" class="btn btn-primary btn-sm">Procedia</a> <a href="https://publications.waset.org/abstracts/15995.pdf" target="_blank" class="btn btn-primary btn-sm">PDF</a> <span class="bg-info text-light px-1 py-1 float-right rounded"> Downloads <span class="badge badge-light">363</span> </span> </div> 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