Kolin’in Merkezi ve Periferik Kolinerjik Nöronlarda ve Kolinerjik İletimdeki İşlevi

Kolin bir kuaterner amin olup, nörotrasmitter asetilkolinin ve membranın temel yapılarından fosfotidilkolin’in öncül maddesidir. Kolin ayrıca vücutta, metionin ve s-adenosilmetionin rejenerasyonu için gerekli metil guruplarının vericisi olan, betaine de metabolize olur. Bu derlemede esas olarak kolin’in cholinergic noronal görevlerindeki rolü üzerinde durulacaktır. Kolinerjik nöronların asetilkolin sentezi için kulandıkları kolin esas olarak kaynağı dolaşımdır. Dolaşımdaki kolin’in düzeyi 6-8 saatlik açlık sonrası 10 μM kadardır. Bu düzey yemek sonrası, gıdalardaki kolin‘in miktarına göre, 20-60 μM kadar yükselebilir. Farmakolojik dozlarda tedavi ile de kan kolin düzeyi 200-300 μM kadar yükselebilir. Kolin’i asetilkoline dönüştüren enzim kolinasetiltrasferaz enzimi substratı kolini zayıf bir şekilde doyurulmuş olduğundan plazmada kolin düzeyinin yükselmesi asetilkolin sentezini arttırır. Kolin, yeterince yüksek düzeylerinde (0,5-100 mM gibi), muskarinik ve nikotinik asetikolin reseptörleri ile agonist olarak da etkileşir. Kolin tedavisi nörotrasmitter asetilkolin’in sentez ve salıverilmesinde hızlanma ve merkezi ve periferik muskarinik ve nikotinik kolinerjik iletide yükselme ile sonuçlanır. Kolin, burada tartışılacak olan, kolinerjik nitelikte birçok fizyolojik, farmakolojik ve nörokimyasal etkiler oluşturur

Dietary Crude Lecithin Increases Systemic Availability of Dietary Docosahexaenoic Acid with Combined Intake in Rats

Crude lecithin, a mixture of mainly phospholipids, potentially helps to increase the systemic availability of dietary omega-3 polyunsaturated fatty acids (n-3 PUFA), such as docosahexaenoic acid (DHA). Nevertheless, no clear data exist on the effects of prolonged combined dietary supplementation of DHA and lecithin on RBC and plasma PUFA levels. In the current experiments, levels of DHA and choline, two dietary ingredients that enhance neuronal membrane formation and function, were determined in plasma and red blood cells (RBC) from rats after dietary supplementation of DHA-containing oils with and without concomitant dietary supplementation of crude lecithin for 2–3 weeks. The aim was to provide experimental evidence for the hypothesized additive effects of dietary lecithin (not containing any DHA) on top of dietary DHA on PUFA levels in plasma and RBC. Dietary supplementation of DHA-containing oils, either as vegetable algae oil or as fish oil, increased DHA, eicosapentaenoic acid (EPA), and total n-3 PUFA, and decreased total omega-6 PUFA levels in plasma and RBC, while dietary lecithin supplementation alone did not affect these levels. However, combined dietary supplementation of DHA and lecithin increased the changes induced by DHA supplementation alone. Animals receiving a lecithin-containing diet also had a higher plasma free choline concentration as compared to controls. In conclusion, dietary DHA-containing oils and crude lecithin have synergistic effects on increasing plasma and RBC n-3 PUFA levels, including DHA and EPA. By increasing the systemic availability of dietary DHA, dietary lecithin may increase the efficacy of DHA supplementation when their intake is combined.Nutricia Researc

Comparison of Self-reported and Measured Height, Weight and BMI in Turkish University Students

Accuracy and validity of self-reported height and weight, and body image satisfaction have not been yet evaluated particularly in young adult population in Turkey. The aim of the study was to establish the differences between self-reported and measured height and weight, and body mass index (BMI). The study was conducted on 617 university students (304 males and 313 females) aged 17–30 years from Ankara and Sivas, Turkey. Height and weight were measured and obtained by a questionnaire. From both measured and self-reported values for accuracy absolute differences were calculated. BMI was calculated from both self-reported and m

Feel-Good Requirements: Neurophysiological and Psychological Design Criteria of Affective Touch for (Assistive) Robots

Previous research has shown the value of the sense of embodiment, i.e., being able to integrate objects into one's bodily self-representation, and its connection to (assistive) robotics. Especially, tactile interfaces seem essential to integrate assistive robots into one's body model. Beyond functional feedback, such as tactile force sensing, the human sense of touch comprises specialized nerves for affective signals, which transmit positive sensations during slow and low-force tactile stimulations. Since these signals are extremely relevant for body experience as well as social and emotional contacts but scarcely considered in recent assistive devices, this review provides a requirement analysis to consider affective touch in engineering design. By analyzing quantitative and qualitative information from engineering, cognitive psychology, and neuroscienctific research, requirements are gathered and structured. The resulting requirements comprise technical data such as desired motion or force/torque patterns and an evaluation of potential stimulation modalities as well as their relations to overall user experience, e.g., pleasantness and realism of the sensations. This review systematically considers the very specific characteristics of affective touch and the corresponding parts of the neural system to define design goals and criteria. Based on the analysis, design recommendations for interfaces mediating affective touch are derived. This includes a consideration of biological principles and human perception thresholds which are complemented by an analysis of technical possibilities. Finally, we outline which psychological factors can be satisfied by the mediation of affective touch to increase acceptance of assistive devices and outline demands for further research and development

Cytidine and Uridine Increase Striatal CDP-Choline Levels Without Decreasing Acetylcholine Synthesis or Release

SUMMARY Aims: Treatments that increase acetylcholine release from brain slices decrease the synthesis of phosphatidylcholine by, and its levels in, the slices. We examined whether adding cytidine or uridine to the slice medium, which increases the utilization of choline to form phospholipids, also decreases acetylcholine levels and release. Methods: We incubated rat brain slices with or without cytidine or uridine (both 25-400 µM), and with or without choline (20-40 µM), and measured the spontaneous and potassium-evoked release of acetylcholine. Results: Striatal slices stimulated for 2 h released 2650 ± 365 pmol of acetylcholine per mg protein when incubated without choline, or 4600 ± 450 pmol/mg protein acetylcholine when incubated with choline (20 µM). Adding cytidine or uridine (both 25-400 µM) to the media failed to affect acetylcholine release whether or not choline was also added, even though the pyrimidines (400 µM) did enhance choline`s utilization to form CDP-choline by 89 or 61%, respectively. The pyrimidines also had no effect on acetylcholine release from hippocampal and cortical slices. Cytidine or uridine also failed to affect acetylcholine levels in striatal slices, nor choline transport into striatal synaptosomes. Conclusion: These data show that cytidine and uridine can stimulate brain phosphatide synthesis without diminishing acetylcholine synthesis or release

Examination of Cognitive Functions and Hippocampal Synaptophysin Levels in an Experimental Schizophrenia Model

Şizofreni pozitif, negatif ve bilişsel belirtiler ile seyreden kronik bir beyin hastalığıdır. Bilişsel belirtiler hastalığın prodromal döneminden itibaren gözlenebilmektedir. Bu çalışmanın amacı irkilme refleksininin ön uyaran aracılı inhibisyonu (ÖUAİ) ile oluşturulan deneysel şizofreni modelinde sıçanların bilişsel fonksiyonlarını ve hipokampal presinaptik proteinlerden sinaptofizin düzeylerini araştırmaktır. Çalışmada 30 adet erkek Wistar türü sıçanlar bazal ÖUAİ ölçümüne tabi tutulmuş ve bu değerlere göre düşükten yükseğe sıralanmıştır. İlk 10 sıçan “düşük” ve son 10 sıçan “yüksek” inhibisyonlu grup olarak ayrıldıktan sonra 5 gün boyunca Morris Su Tankı (MST) testine tabi tutulmuştur. Testin bitiminde sıçanlar sakrifiye edilerek hipokampus bölgeleri eksize edilmiş ve hipokampal presinaptik proteinlerden sinaptofizin Western Blot yöntemiyle analiz edilmiştir. Sonuçlara göre her iki grubun öğrenme düzeyleri arasında fark bulunmaz iken ve hafıza fonksiyonlarının platform alanından geçme sıklığı (p<0,05) ve platform alanında geçirilen süre parametreleri (p<0,05) düşük ÖUAİ gruptaki sıçanlarda anlamlı olarak daha düşük bulunmuştur. Sinaptofizin düzeyleri de benzer şekilde düşük ÖUAİ grubundaki sıçanlarda anlamlı olarak (p<0,01) düşük tespit edilmiştir. Çalışmamızın sonuçları yüksek ÖUAİ değerine sahip sıçanlarla kıyaslandığında ÖUAİ değerleri düşük olan sıçanların bazı bilişsel fonksiyonlarının ve hipokampal presinaptik proteinlerden sinaptofizin düzeylerinin anlamlı olarak daha düşük olduğunu göstermektedir. Bu sonuçlar aynı zamanda uzun zamandır şizofreni çalışmalarında güvenilir bir yöntem olarak kullanılan ÖUAİ testinin insan ve hayvan çalışmalarındaki benzer sonuçlarına vurgu yaparak şizofreni araştırmalarındaki önemini desteklemiştir.Schizophrenia is a chronic brain disease and is clinically characterized by positive, negative and cognitive symptoms. Cognitive symptoms can be observed starting from the prodromal period of the disease. The aim of this study is to investigate the cognitive functions of rats and hippocampal levels of the presynaptic protein synaptophysin in an experimental schizophrenia model created by prepulse-mediated inhibition (PPI) of the startle reflex. In the study, 30 male Wistar type rats were subjected to basal PPI measurements and were ranked from low to high according to these values. After the first 10 rats were divided into the "low" and the last 10 rats into the "high" inhibition group, they were subjected to the Morris Water Maze (MWM) test for 5 days. At the end of the test, the rats were sacrificed, hippocampus regions were excised, and the presynaptic synaptophysin protein was analyzed by Western Blot method. According to the results, while there was no difference between the learning levels of both groups, the frequency of memory functions frequency to cross the platform area (p <0.05) and time spent in the platform area (p <0.05) parameters were found to be significantly lower in rats in the low PPI group. Synaptophysin levels were similarly found to be significantly (p<0.01) lower in rats in the low PPI group. The results of our study show that some cognitive functions and presynaptic protein synaptophysin levels are significantly lower in rats with low PPI values compared to those with high PPI values. These results also supported the importance of the PPI test, which has been used as a reliable method in schizophrenia research for a long time, by emphasizing its comparable outcomes in human and animal studies of schizophrenia

Dietary Crude Lecithin Increases Systemic Availability of Dietary Docosahexaenoic Acid with Combined Intake in Rats

Crude lecithin, a mixture of mainly phospholipids, potentially helps to increase the systemic availability of dietary omega-3 polyunsaturated fatty acids (n-3 PUFA), such as docosahexaenoic acid (DHA). Nevertheless, no clear data exist on the effects of prolonged combined dietary supplementation of DHA and lecithin on RBC and plasma PUFA levels. In the current experiments, levels of DHA and choline, two dietary ingredients that enhance neuronal membrane formation and function, were determined in plasma and red blood cells (RBC) from rats after dietary supplementation of DHA-containing oils with and without concomitant dietary supplementation of crude lecithin for 2–3 weeks. The aim was to provide experimental evidence for the hypothesized additive effects of dietary lecithin (not containing any DHA) on top of dietary DHA on PUFA levels in plasma and RBC. Dietary supplementation of DHA-containing oils, either as vegetable algae oil or as fish oil, increased DHA, eicosapentaenoic acid (EPA), and total n-3 PUFA, and decreased total omega-6 PUFA levels in plasma and RBC, while dietary lecithin supplementation alone did not affect these levels. However, combined dietary supplementation of DHA and lecithin increased the changes induced by DHA supplementation alone. Animals receiving a lecithin-containing diet also had a higher plasma free choline concentration as compared to controls. In conclusion, dietary DHA-containing oils and crude lecithin have synergistic effects on increasing plasma and RBC n-3 PUFA levels, including DHA and EPA. By increasing the systemic availability of dietary DHA, dietary lecithin may increase the efficacy of DHA supplementation when their intake is combined.Nutricia Researc

Cardiovascular, metabolic and neuroendocrine effects of CDP-CHOLINE

Bu çalışmada sıçanlara periton içi (i.p.) yolla verilen CDP-kolin'in kardiyovasküler, metabolik ve nöroendokrin etkileri incelendi. İ.p. yolla zerk edilen CDP-kolin (105, 210, 315 ve 473 mg/kg) kan basıncını doza ve zamana bağlı olarak 17-35 mm Hg kadar artırırken kalp hızını doza ve zamana bağlı olarak 32-53 atım/dakika kadar azalttı. CDP-kolin'in kan basıncını yükseltici etkisi atropin metil nitrat veya hekzametonyum gibi kolinerjik reseptör antagonistleri ve prazosin, yohimbin veya propranolol gibi adrenerjik reseptör antagonistleri ile ön tedaviyi takiben ya da bilateral adrenalektomi sonrası değişmedi. CDP-kolin'in bradikardik etkisi ise, atropin metil nitrat veya prazosin ön tedavisi sonrası bloke oldu, hekzametonyum ön tedavisini takiben tersine döndü. Bradikardik etki yohimbin ön tedavisinden ve bilateral adrenalektomiden etkilenmedi. Propranolol ön tedavisi sonrası kalp atım hızında düşüş gözlendi ve CDP-kolin verilmesinden sonra da bu düşme değişmedi. CDP-kolin (105, 210 ve 315 mg/kg; i.p.) serum glukoz düzeylerini zamana bağlı olarak 16-29 mg/dl kadar artırdı. Hekzametonyum ön tedavisi bu hiperglisemik etkiyi bloke ederken atropin metil nitrat değiştirmedi. CDP-kolin'in hiperglisemik etkisi yohimbin ön tedavisi veya bilateral adrenalektomi ile bloke olurken, propranolol ön tedavisi hiperglisemik etkiyi değiştirmedi. CDP-kolin (210 ve 315 mg/kg; i.p.) zerkini takiben 10. dakikada plazma adrenalin düzeyleri anlamlı olarak arttı. 315 mg/kg CDP-kolin sonrasında 5, 10, ve 20. dakikalarda plazma noradrenalin düzeyleri anlamlı olarak arttı. 315 ve 473 mg/kg dozlarında serum insülin düzeyleri ve tüm dozlarda (105, 210, 315 ve 473 mg/kg) plazma glukagon düzeyleri zerki takiben 10. dakikada anlamlı şekilde arttı. Sonuç olarak; CDP-kolin çeşitli kardiyovasküler, metabolik ve nöroendokrin etkilere sahiptir. CDP-kolin'in tüm bu etkilerinde açığa çıkan kolin'in yol açtığı kolinerjik aktivasyonun aracılığı rol oynayabilir.In this study cardiovascular, metabolic and neuroendocrine effects of CDP-choline when given intraperitoneally (i.p.) to rats were investigated. I.p. injected CDP-choline (105, 210, 315 and 473 mg/kg) increased blood pressure dose- and time-dependently by means of 17-35 mm Hg, while it decreased heart rate dose- and time-dependently by means of 32-53 beats/minute. The hypertensive effect of CDP-choline didn't change following pretreatment with the cholinergic receptor antagonists atropine methyl nitrate or hexamethonium and the adrenergic receptor antagonists prazosin, yohimbine or propranolol or following bilateral adrenalectomy. The bradycardic effect of CDP-choline was blocked after atropine methyl nitrate or prazosin pretreatment, reversed following hexamethonium pretreatment. Bradycardic effect wasn't effected by yohimbine pretreatment or bilateral adrenalectomy. A fall in heart rate was observed after propranolol and this fall didn't change after CDP-choline injection. CDP-choline (105, 210 ve 315 mg/kg; i.p.) increased serum glucose levels time-dependently by 16-29 mg/di. While hexamethonium blocked this hyperglycemic effect, atropine methyl nitrate didn't change it. CDP-choline's hyperglycemic effect was blocked by yohimbine pretreatment or by bilateral adrenalectomy, while propranolol did not effect the hyperglycemic effect. CDP-choline (210 ve 315 mg/kg; i.p.) increased plasma adrenaline levels significantly at 10th minute. CDP-choline at the dose of 315 mg/kg increased plasma noradrenaline levels significantly at 5, 10 and 20th minutes. 315 and 473 mg/kg CDP-choline increased serum insulin and all tested doses (105, 210, 315 ve 473 mg/kg) of CDP-choline increased plasma glucagon levels significantly 10 minutes following injection. As a result; CDP-choline has some cardiovascular, metabolic and neuroendocrine effects. Mediation of cholinergic activation caused by choline moiety may play a role in all these effects of CDP-choline

Antioxidative effects of uridine in a neonatal rat model of hyperoxic brain injury

Background/aim: Premature birth is a major problem that results in an increased risk of mortality and morbidity. The management of such infants consists of supraphysiological oxygen therapy, which affects brain development due, in part, to the deterioration caused by reactive oxygen species (ROS). We showed previously that exogenously administered uridine provides neuroprotection in a neonatal rat model of hyperoxic brain injury. Hence, the aim of the present study was to investigate the effects of uridine on ROS in the same setting. Materials and methods: Hyperoxic brain injury was induced by subjecting a total of 53 six-day-old rat pups to 80% oxygen (the hyperoxia group) for a period of 48 h. The pups in the normoxia group continued breathing room air (21% oxygen). Normoxia + saline or hyperoxia + saline or hyperoxia + uridine 100 mg/kg or hyperoxia + uridine 300 mg/kg or hyperoxia + uridine 500 mg/kg was injected intraperitoneally (i. p.) 15 min prior to the hyperoxia procedure. The pups were decapitated and the brains were homogenized to analyze superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), myeloperoxidase (MPO), and malondialdehyde (MDA) enzymes as well as DJ-1 (protein deglycase DJ-1) — an oxidative stress-sensitive protein. Results: Hyperoxia-induced may cause overproduction of oxygen radicals and the oxidant/antioxidant balance may be disturbed in the brain. Brain MPO and MDA levels were significantly increased in saline-receiving pups exposed to hyperoxia. Brain SOD and GSH-Px levels were significantly decreased in saline-receiving pups exposed to hyperoxia. Our results showed that uridine administration prevented the hyperoxia-induced decrease in SOD and GSH-Px while counteracting the hyperoxia-induced increase in MPO and MDA in a dose-dependent manner. Uridine also increased the DJ-1 levels in brains of rat pups subjected to hyperoxia. Conclusion: These data suggest that uridine exhibits antioxidative properties which may mediate the protective effects of uridine in a neonatal rat model of hyperoxic brain injury.Bursa Uludag University Scientific Research Projects Counci