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Academic literature on the topic 'Memory Disorders Rats. Glucose Neurotransmitters'
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Journal articles on the topic "Memory Disorders Rats. Glucose Neurotransmitters"
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Dienel, Gerald A. "Brain Glucose Metabolism: Integration of Energetics with Function." Physiological Reviews 99, no. 1 (January 1, 2019): 949–1045. http://dx.doi.org/10.1152/physrev.00062.2017.
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Glucose is the long-established, obligatory fuel for brain that fulfills many critical functions, including ATP production, oxidative stress management, and synthesis of neurotransmitters, neuromodulators, and structural components. Neuronal glucose oxidation exceeds that in astrocytes, but both rates increase in direct proportion to excitatory neurotransmission; signaling and metabolism are closely coupled at the local level. Exact details of neuron–astrocyte glutamate–glutamine cycling remain to be established, and the specific roles of glucose and lactate in the cellular energetics of these processes are debated. Glycolysis is preferentially upregulated during brain activation even though oxygen availability is sufficient (aerobic glycolysis). Three major pathways, glycolysis, pentose phosphate shunt, and glycogen turnover, contribute to utilization of glucose in excess of oxygen, and adrenergic regulation of aerobic glycolysis draws attention to astrocytic metabolism, particularly glycogen turnover, which has a high impact on the oxygen–carbohydrate mismatch. Aerobic glycolysis is proposed to be predominant in young children and specific brain regions, but re-evaluation of data is necessary. Shuttling of glucose- and glycogen-derived lactate from astrocytes to neurons during activation, neurotransmission, and memory consolidation are controversial topics for which alternative mechanisms are proposed. Nutritional therapy and vagus nerve stimulation are translational bridges from metabolism to clinical treatment of diverse brain disorders.
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Ahmed, Nawal A., Nasr M. Radwan, Heba S. Aboul Ezz, Yasser A. Khadrawy, and Noha A. Salama. "The chronic effect of pulsed 1800 MHz electromagnetic radiation on amino acid neurotransmitters in three different areas of juvenile and young adult rat brain." Toxicology and Industrial Health 34, no. 12 (October 21, 2018): 860–72. http://dx.doi.org/10.1177/0748233718798975.
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The extensive use of mobile phones worldwide has raised increasing concerns about the effects of electromagnetic radiation (EMR) on the brain due to the proximity of the mobile phone to the head and the appearance of several adverse neurological effects after mobile phone use. It has been hypothesized that the EMR-induced neurological effects may be mediated by amino acid neurotransmitters. Thus, the present study investigated the effect of EMR (frequency 1800 MHz, specific absorption rate 0.843 W/kg, power density 0.02 mW/cm2, modulated at 217 Hz) on the concentrations of amino acid neurotransmitters (glutamic acid, aspartic acid, gamma aminobutyric acid, glycine, taurine, and the amide glutamine) in the hippocampus, striatum, and hypothalamus of juvenile and young adult rats. The juvenile and young adult animals were each divided into two groups: control rats and rats exposed to EMR 1 h daily for 1, 2, and 4 months. A subgroup of rats were exposed daily to EMR for 4 months and then left without exposure for 1 month to study the recovery from EMR exposure. Amino acid neurotransmitters were measured in the hippocampus, striatum, and hypothalamus using high-performance liquid chromatography. Exposure to EMR induced significant changes in amino acid neurotransmitters in the studied brain areas of juvenile and young adult rats, being more prominent in juvenile animals. It could be concluded that the alterations in amino acid neurotransmitters induced by EMR exposure of juvenile and young adult rats may underlie many of the neurological effects reported after EMR exposure including cognitive and memory impairment and sleep disorders. Some of these effects may persist for some time after stopping exposure.
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Mahmoud, Sahar, Yasmin Latif, Hisham Orban, Amr Ibrahim, and Jihan Hussein. "Docosahexaenoic acid modulates oxidative stress and monoamines levels in brain of streptozotocin-induced diabetic rats." Acta Facultatis Medicae Naissensis 38, no. 2 (2021): 135–46. http://dx.doi.org/10.5937/afmnai38-28984.
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The prevalence of diabetes mellitus (DM) is increasing in many countries. A lower prevalence of DM type 2 and other glucose metabolism disorders was observed in populations consuming larger amounts of n-3 polyunsaturated fatty acids, existing mainly in fish. Docosahexaenoic acid (DHA) is an important signaling molecule required for the central nervous system continuous maintenance of brain functioning. The aim of this research is to highlight the role of DHA in controlling glycemic measures and modulating the oxidant/antioxidant status and levels of neurotransmitters in brains of diabetic rats. Diabetes was induced with a single s.c. injection of streptozotocin (STZ) (6.0 mg/0.5 ml/100 g body weight). Experimental male Wister rats (n=40) were randomly divided into four groups: control group, DHA, STZ-diabetic, and STZ + DHA. All rats were decapitated after 30 days to evaluate glucose and insulin levels, brain oxidative stress and also to estimate monoamines levels. DHA administration significantly improved fasting blood glucose and insulin levels compared to the DHA+STZ group and decreased 8-hydroxy-2'-deoxyguanosine level in their urine. In addition, DHA treatment to STZ-treated rats showed a decrease in malondialdehyde content and advanced oxidation protein product and significantly increased glutathione content in brains of DHA + STZ-treated rats, and decreased the level of monoamines in rat's brain. To conclude: DHA modulated the elevated oxidative stress and neurotransmitters levels, and also acetylcholinesterase activity in diabetic rat brain via enhancing insulin level in serum
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Han, Xu, Xiaoyan Chen, Xuan Wang, Meirong Gong, Mengjiang Lu, Zhi Yu, Bin Xu, and Jinhong Yuan. "Electroacupuncture at ST36 Improve the Gastric Motility by Affecting Neurotransmitters in the Enteric Nervous System in Type 2 Diabetic Rats." Evidence-Based Complementary and Alternative Medicine 2021 (June 16, 2021): 1–13. http://dx.doi.org/10.1155/2021/6666323.
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Electroacupuncture (EA) can effectively relieve hyperglycemia and gastric emptying disorders in diabetic gastroparesis (DGP). However, the effect of EA on type 2 diabetes mellitus (T2DM) gastroparesis and its mechanism in the enteric nervous system (ENS) are rarely studied. We investigated the therapeutic effect of EA at ST36 and its effect on the main inhibitory and excitatory neurotransmitters in the ENS in DGP rats. Male Sprague-Dawley (SD) rats were fed a high-fat diet for 2 weeks and injected with streptozotocin (STZ) at 35 mg/kg to induce T2DM. T2DM rats were divided into the diabetic mellitus (DM) group and the EA group. The control (CON) group comprised normal rats without any intervention. EA treatment was started 6 weeks after the induction of DM and continued for 5 weeks. The body weight and food intake of the rats were recorded every week. Blood glucose, insulin, glucose tolerance, gastric emptying, and antral motility were measured after treatment. The expression of protein gene product 9.5 (PGP9.5), neuronal nitric oxide synthase (nNOS), and choline acetyltransferase (ChAT) in gastric antrum were quantified by western blotting and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). The T2DM gastroparesis model was successfully established. EA treatment reduced the body weight, food intake, and blood glucose; improved glucose intolerance and insulin resistance; increased the gastric emptying rate, the mean antral pressure, and the amplitude of antral motility; and decreased the frequency of antral motility compared with those in the DM group. EA treatment increased the expression level of nNOS, ChAT, and PGP9.5 proteins, and nNOS and ChAT mRNA. The results suggested that EA at ST36 could ameliorate DGP, partly restore the damage to general neurons, and increase nNOS and ChAT in the gastric antrum. EA improved DGP partly via reducing the loss of inhibitory and excitatory neurotransmitters in the ENS.
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Salmina, A. B., N. A. Yauzina, N. V. Kuvacheva, M. M. Petrova, T. Ye Taranushenko, N. A. Malinovskaya, O. L. Lopatina, et al. "INSULIN AND INSULIN RESISTANCE: NEW MOLECULE MARKERS AND TARGET MOLECULE FOR THE DIAGNOSIS AND THERAPY OF DISEASES OF THE CENTRAL NERVOUS SYSTEM." Bulletin of Siberian Medicine 12, no. 5 (October 28, 2013): 104–18. http://dx.doi.org/10.20538/1682-0363-2013-5-104-118.
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The review summarizes current data on the role of insulin in the regulation of t glucose metabolism in the central nervous system at physiologic and pathologic conditions. For many years, the brain has been considered as an insulin-independent organ which utilizes glucose without insulin activity. However, it is become clear now that insulin not only regulates glucose transport and metabolism, but also has modulatory efftects in impact on excitability, proliferation and differentiation of brain progenitor cells, synaptic plasticity and memory formation, secretion of neurotransmitters, apoptosis. We have critically reviewed literature information and our own data on the role of insulin and insulin resistance in neuron-glia metabolic coupling, regulation of NAD+ metabolism and action of NAdependent enzymes, neurogenesis, brain development in (patho)physiological conditions. The paper clarifies interrelations between alterations in glucose homeostasis, development of insulin resistance and development of neurodegeneration (Alzheimer's disease and Parkinson's disease), autism, stroke, and depression. We discuss the application of novel molecular markers of insulin resistance (adipokines, α-hydroxybutyrate, BDNF, insulin-regulated aminopeptidase, provasopressin) and molecular targets for diagnostics and treatment of brain disorders associated with insulin resistance.
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Cui, Shaoyang, Mingzhu Xu, Jianting Huang, Qing Mei Wang, Xinsheng Lai, Binbin Nie, Baoci Shan, Xun Luo, John Wong, and Chunzhi Tang. "Cerebral Responses to Acupuncture at GV24 and Bilateral GB13 in Rat Models of Alzheimer’s Disease." Behavioural Neurology 2018 (2018): 1–10. http://dx.doi.org/10.1155/2018/8740284.
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Acupuncture has been widely used in China to treat neurological diseases including Alzheimer’s disease (AD). However, its mechanism remains unclear. In the present study, eighty healthy Wistar rats were divided into a normal control group (n=15) and premodel group (n=65). Forty-five rats that met the criteria for the AD model were then randomly divided into the model group (MG), the nonacupoint group (NG), and the acupoint group (AG). All rats received positron emission tomography (PET) scanning, and the images were analyzed with Statistical Parametric Mapping 8.0. MG exhibited hypometabolism in the olfactory bulb, insular cortex, orbital cortex, prelimbic cortex, striatum, parietal association cortex, visual cortex, cingulate gyrus, and retrosplenial cortex. AG exhibited prominent and extensive hypermetabolism in the thalamus, hypothalamus, bed nucleus of the stria terminalis, cerebral peduncle, midbrain tegmentum, and pontine tegmentum compared to NG. These results demonstrated that acupuncturing at GV24 and bilateral GB13 acupoints may improve the learning and memory abilities of the AD rats, probably via altering cerebral glucose metabolism (CGM) in the hypothalamus, thalamus, and brain stem. The observed effects of acupuncture may be caused by regulating the distribution of certain kinds of neurotransmitters and enhancing synaptic plasticity.
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Lange, Klaus W., Joachim Hauser, Ivo Kaunzinger, Yukiko Nakamura, Andreas Reissmann, Ewelina Stollberg, Jianjun Guo, and Shiming Li. "Chronic increase in sugar consumption and visual attention in Wistar rats." Journal of Food Bioactives 3 (September 30, 2018): 161–67. http://dx.doi.org/10.31665/jfb.2018.3159.
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High sugar consumption is known to elevate the risk of obesity and related metabolic disturbances, but far less is known about its effects on cognition, learned behavior and mental health. Experimental findings in rodents indicate that increased sugar intake can induce cognitive impairment, most consistently in regard to memory functions. Studies examining the effects of an increase in dietary sugars on attention are lacking. The present study investigated the effects on visual attention of chronic high intake of sucrose and glucose in Wistar rats. Two groups of Wistar dams and their offspring were fed either a diet high in sugar, containing a high percentage of sucrose and glucose, or a standard sucrose/glucose diet. Attention was examined using a 3-choice-serial-reactiontime task. The present results demonstrated detrimental effects of high pre- and postnatal sugar consumption on visual attention in rats. The previously demonstrated memory impairments following increased sugar consumption may be mediated, at least partly, by attentional deficits. Future studies should investigate the translational relevance of these findings in humans, particularly in regard to mental disorders such as attention deficit/hyperactivity disorder (ADHD). Emerging evidence suggests that the mechanisms underlying the behavioral impairments related to diets high in sugar and/or fat may include neuroinflammation, changes of the blood–brain barrier and altered levels of brain-derived neurotrophic factor (BDNF). The elucidation of these mechanisms requires further investigations.
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Bockaert, Joël, and Philippe Marin. "mTOR in Brain Physiology and Pathologies." Physiological Reviews 95, no. 4 (October 2015): 1157–87. http://dx.doi.org/10.1152/physrev.00038.2014.
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TOR (target of rapamycin) and its mammalian ortholog mTOR have been discovered in an effort to understand the mechanisms of action of the immunosuppressant drug rapamycin extracted from a bacterium of the Easter Island (Rapa Nui) soil. mTOR is a serine/threonine kinase found in two functionally distinct complexes, mTORC1 and mTORC2, which are differentially regulated by a great number of nutrients such as glucose and amino acids, energy (oxygen and ATP/AMP content), growth factors, hormones, and neurotransmitters. mTOR controls many basic cellular functions such as protein synthesis, energy metabolism, cell size, lipid metabolism, autophagy, mitochondria, and lysosome biogenesis. In addition, mTOR-controlled signaling pathways regulate many integrated physiological functions of the nervous system including neuronal development, synaptic plasticity, memory storage, and cognition. Thus it is not surprising that deregulation of mTOR signaling is associated with many neurological and psychiatric disorders. Preclinical and preliminary clinical studies indicate that inhibition of mTORC1 can be beneficial for some pathological conditions such as epilepsy, cognitive impairment, and brain tumors, whereas stimulation of mTORC1 (direct or indirect) can be beneficial for other pathologies such as depression or axonal growth and regeneration.
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Ye, Minsook, Bong Hee Han, Jin Su Kim, Kyungsoo Kim, and Insop Shim. "Neuroprotective Effect of Bean Phosphatidylserine on TMT-Induced Memory Deficits in a Rat Model." International Journal of Molecular Sciences 21, no. 14 (July 11, 2020): 4901. http://dx.doi.org/10.3390/ijms21144901.
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Background: Trimethyltin (TMT) is a potent neurotoxin affecting various regions of the central nervous system, including the neocortex, the cerebellum, and the hippocampus. Phosphatidylserine (PS) is a membrane phospholipid, which is vital to brain cells. We analyzed the neuroprotective effects of soybean-derived phosphatidylserine (Bean-PS) on cognitive function, changes in the central cholinergic systems, and neural activity in TMT-induced memory deficits in a rat model. Methods: The rats were randomly divided into an untreated normal group, a TMT group (injected with TMT + vehicle), and a group injected with TMT + Bean-PS. The rats were treated with 10% hexane (TMT group) or TMT + Bean-PS (50 mg·kg−1, oral administration (p.o.)) daily for 21 days, following a single injection of TMT (8.0 mg/kg, intraperitoneally (i.p.)). The cognitive function of Bean-PS was assessed using the Morris water maze (MWM) test and a passive avoidance task (PAT). The expression of acetylcholine transferase (ChAT) and acetylcholinesterase (AchE) in the hippocampus was assessed via immunohistochemistry. A positron emission tomography (PET) scan was used to measure the glucose uptake in the rat brain. Results: Treatment with Bean-PS enhanced memory function in the Morris water maze (MWM) test. Consistent with the behavioral results, treatment with Bean-PS diminished the damage to cholinergic cells in the hippocampus, in contrast to those of the TMT group. The TMT+Bean-PS group showed elevated glucose uptake in the frontal lobe of the rat brain. Conclusion: These results demonstrate that Bean-PS protects against TMT-induced learning and memory impairment. As such, Bean-PS represents a potential treatment for neurodegenerative disorders, such as Alzheimer’s disease.
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Bhuvanendran, Saatheeyavaane, Siti Najmi Syuhadaa Bakar, Yatinesh Kumari, Iekhsan Othman, Mohd Farooq Shaikh, and Zurina Hassan. "Embelin Improves the Spatial Memory and Hippocampal Long-Term Potentiation in a Rat Model of Chronic Cerebral Hypoperfusion." Scientific Reports 9, no. 1 (October 10, 2019). http://dx.doi.org/10.1038/s41598-019-50954-y.
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Abstract Alzheimer’s disease (AD) is the second most occurring neurological disorder after stroke and is associated with cerebral hypoperfusion, possibly contributing to cognitive impairment. In the present study, neuroprotective and anti-AD effects of embelin were evaluated in chronic cerebral hypoperfusion (CCH) rat model using permanent bilateral common carotid artery occlusion (BCCAO) method. Rats were administered with embelin at doses of 0.3, 0.6 or 1.2 mg/kg (i.p) on day 14 post-surgery and tested in Morris water maze (MWM) followed by electrophysiological recordings to access cognitive abilities and synaptic plasticity. The hippocampal brain regions were extracted for gene expression and neurotransmitters analysis. Treatment with embelin at the doses of 0.3 and 0.6 mg/kg significantly reversed the spatial memory impairment induced by CCH in rats. Embelin treatment has significantly protected synaptic plasticity impairment as assessed by hippocampal long-term potentiation (LTP) test. The mechanism of this study demonstrated that embelin treatment alleviated the decreased expression of BDNF, CREB1, APP, Mapt, SOD1 and NFκB mRNA levels caused by CCH rats. Furthermore, treatment with embelin demonstrated neuromodulatory activity by its ability to restore hippocampal neurotransmitters. Overall these data suggest that embelin improve memory and synaptic plasticity impairment in CCH rats and can be a potential drug candidate for neurodegenerative disease-related cognitive disorders.
Dissertations / Theses on the topic "Memory Disorders Rats. Glucose Neurotransmitters"
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Stefani, Mark Renato. "Central K-ATP channels modulate rat spontaneous alternation behavior : a potential mechanism for the memory-enhancing effects of D-Glucose /." 1999. http://wwwlib.umi.com/dissertations/fullcit/9916349.
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