Search results for “glutamate

About 6 results in articles

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6 articles

Exercise and Vitamin D Supplementation Modify Spleen Morphology in Lean, but not, in Monosodium-Glutamate-Obese Rats

Aug 2019 DOI 10.14302/issn.2578-2371.jslr-19-2819
Maria Guareschi ZoéCorresponding author Laboratory of Endocrine and Metabolic Physiology, University of West Parana (Unioeste), Cascavel, PR, Brazil. +55 4532203257.

An experimental study examines how exercise and vitamin D supplementation affect spleen morphology in lean versus MSG‑obese rats, discussing immunologic implications.

Evidence that N-acetylaspartylglutamate is the Astrocyte-Targeted Neurovascular Coupling Agent that Regulates Slow Tonic Control of Brain Blood Flow

Jun 2016 DOI 10.14302/issn.2572-5424.jgm-16-1028
H Baslow MorrisCorresponding author Center for Biomedical Imaging and Neuromodulation, Nathan Kline Institute for Psychiatric Research, 140 Old Orangeburg Road, Orangeburg, NY, 10962, USA.

N-acetylaspartylglutamate (NAAG) is the highest concentration dipeptide present in brain. It is found primarily in neurons but its function is unclear. NAAG is synthesized by neurons from N-acetylaspartate and glutamate (Glu), maintained at mM concentrations and is released non-synaptically to extracellular fluid (ECF). NAAG is a non-excitatory form of Glu, and is targeted to the metabotropic group II Glu receptor 3 (mGluR3) on the surface of astrocytes. After docking with the receptor, Glu is released by the action of NAAG peptidase. Previously, it was shown for the first time that an NAAG-peptidase inhibitor reduced global cerebral blood flow (CBF) in mouse brain but did not affect their physical performance. Recently, it has been demonstrated that there are two separate systems involved in neurovascular coupling by astrocytes, one is a rapid focal phasic response providing energy for stimulation-induced neuronal activity, and the other a slower global tonic response providing energy for ongoing metabolic activities. Many neurovascular coupling mechanisms are known that regulate phasic changes in CBF, but how the brain accomplishes tonic control is unknown. In this paper we bring together two separate lines of inquiry, the decades’ long search for the function of NAAG, and the more recent search for the mechanism of tonic neurovascular control. Herein, we present evidence that NAAG is the neurovascular coupling agent that regulates tonic changes in CBF via the astrocyte mGluR3-NAAG peptidase connection.

ADHD And Care Open Access

Trading on Impulse: The Role of ADHD, Impulsivity, and Gender in Financial Risk and Investment Outcomes

Aug 2025 DOI 10.14302/issn.3066-8042.jac-25-5652
Amiri DavoudCorresponding author

Background Attention-deficit/hyperactivity disorder (ADHD) in adulthood is increasingly recognized not only as a psychiatric condition but also as a trait with behavioral and occupational implications—particularly in high-stakes, fast-paced financial environments. Traits such as impulsivity, sensation seeking, and altered reward sensitivity may influence decision-making among individuals engaged in stock trading or high-risk investment professions. Objective This systematic review and meta-analytic synthesis aims to investigate the relationship between ADHD, impulsivity, gender differences, and financial risk behavior, with a particular focus on decision-making outcomes in real or simulated trading contexts. Methods Seventeen peer-reviewed studies published between 2008 and 2025 were included. Studies employed behavioral experiments, fMRI paradigms, neurochemical analysis (e.g., glutamate levels), and ecological financial assessments to examine impulsive traits and investment behaviors among adults with and without ADHD. Both clinical samples and occupational cohorts (e.g., brokers, retail investors) were analyzed. The analysis followed PRISMA 2020 guidelines. Results ADHD symptoms—particularly impulsivity and reward hypersensitivity—were associated with increased delay discounting, higher risk-taking, and diminished cognitive control in financial tasks. Neuroimaging data revealed hypoactivation in prefrontal control regions and hyperactivation in reward-related circuits (e.g., ventral striatum). Gender-stratified analyses showed that males with ADHD displayed stronger preference for immediate rewards, higher portfolio turnover, and greater volatility. Preliminary evidence also suggests an overrepresentation of ADHD traits in high-frequency trading roles. Conclusion ADHD-related impulsivity significantly modulates financial risk behavior, particularly in high-stakes and fast-paced contexts such as trading. A convergence of behavioral, neurobiological, and ecological findings suggests that males with ADHD are disproportionately prone to rapid, high-risk financial decisions, whereas females may demonstrate greater regulatory control. These insights underscore the need for gender-sensitive interventions, occupational screening, and tailored psychoeducation. As financial environments become increasingly automated and fast-paced, understanding the neurocognitive vulnerabilities of individuals with ADHD may not only protect personal outcomes but also enhance systemic financial stability.

Evaluation of Cardiac Performance after Treatment with the Biofield Energy Treated Proprietary Test Formulation on L-NAME and High Fat Diet-Induced Cardiovascular Disorders in Sprague Dawley Rats

Jul 2021 DOI 10.14302/issn.2329-9487.jhc-21-3848
Jana SnehasisCorresponding author Trivedi Science Research Laboratory Pvt. Ltd., Thane (W), Maharashtra, India.

Study was aimed to evaluate effect of Biofield Treated Proprietary Formulation and Biofield Treatment per se on cardiac performance on NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) and high fat diet (HFD)-induced cardiovascular disorders in Sprague Dawley rats. Nine groups were assigned, in which four were preventive maintenance groups. The constituents of test formulation were divided into two parts; one section was defined as the untreated test formulation, while the other portion of the test formulation and three groups of animals received Biofield Energy Healing Treatment remotely for about 3 minutes by a renowned Biofield Energy Healer, Mr. Mahendra Kumar Trivedi. Systolic blood pressure (SBP) was significantly (p≤0.001) decreased by 13.39%, 14.65%, 17.74%, 14.36%, and 14.69% in the G5, G6, G7, G8, and G9 groups, respectively as compared to disease control (G2) group. Diastolic blood pressure (DBP)was significantly (p≤0.001) reduced by 25.95%, 24.41%, 30.79%, 24.67%, and 25.23% in G5, G6, G7, G8, and G9 groups, respectively than G2. Heart rate (HR) was significantly (p≤0.05) reduced by 6.58%, 8.06%, and 6.99% in G7, G8, and G9 groups, respectively than G2. Total leucocyte count (TLC) count was increased by 12.8% and 17.45% in G5 and G8 groups, respectively than G2 group. Neutrophils and lymphocytes were increased by 60.11% (G8) and 11.49% (G5), respectively than G2. Eosinophils were reduced by 11.11%, 20%, and 15% in G6, G7, and G9 groups, respectively than G2. Total cholesterol was significantly decreased by 22.64% (p≤0.05), 15.78%, 25.56% (p≤0.05), 22.56%, and 34.27% in G5, G6, G7, G8, and G9 groups, respectively than G2. Triglyceride was significantly (p≤0.001) reduced by 34.55%, 43.29%, 55.23%, 28.57%, and 37.28% in G5, G6, G7, G8, and G9 groups, respectively than G2. VLDL level was also significantly (p≤0.001) reduced by 80.81%, 83.61%, 86.82%, 79.19%, and 81.63% in G5, G6, G7, G8, and G9 group, respectively; while LDL was reduced by 20.32% (G9) group than G2. Atherogenic index (AI) was significantly (p≤0.001) decreased by 78.36%, 83.21%, 84.68%, 74.06%, and 72.98% in the G5, G6, G7, G8, and G9 groups, respectively than G2. The level of uric acid (UA) was significantly (p≤0.001) decreased by 57.51%, 52.36%, 45.49%, 43.78%, and 40.77% in the G5, G6, G7, G8, and G9 groups respectively, as compared with the G2 group. Serum glutamate pyruvate transaminases (SGPT) was significantly (p≤0.001) decreased by 45.96%, 48.01%, 37.19%, 37.69%, and 42.93% in the G5, G6, G7, G8, and G9 groups, respectively than G2. Creatine kinase myocardial band (CK-MB) level was significantly reduced by 10.19%, 21.97% (p≤0.01), 10.47%, and 16.94% in the G5, G6, G7, and G9 groups, than G2. Overall, the data suggested significance improvement of heart-related hematology, hepatic, and lipid parameters with respect to various pathological conditions that might be beneficial various types of cardiovascular disorders. Therefore, the results showed the significant slowdown the cardiovascular disease progression and its complications/symptoms in the preventive treatment groups viz. G6, G7, G8, and G9.

Rescuing Canavan Disease by Redirecting Metabolic Processing: Support for the Astrocyte Hypothesis of Canavan Disease Generation and A Possible Human Cure

Apr 2017 DOI 10.14302/issn.2572-5424.jgm-17-1482
H Baslow MorrisCorresponding author Center for Biomedical Imaging and Neuromodulation, Nathan Kline Institute for Psychiatric Research

Canavan disease (CD) is a globally occurring but rare human spongiform leukodystrophy that is associated with inborn errors affecting the activity of aspartoacylase (ASPA), an enzyme highly expressed in oligodendrocytes that hydrolyzes N-acetylaspartate (NAA). Lack of ASPA activity is associated with the inability of oligodendrocytes to build or maintain axon-enveloping myelin sheaths. The primary source of NAA in brain is neurons, cells that synthesize but cannot catabolize it. Neurons also synthesize N-acetylaspartylglutamate (NAAG) from NAA and glutamate but cannot catabolize this substance as well. For their metabolism, these substances are released to extracellular fluid and are metabolized by oligodendrocyte ASPA and astrocyte NAAG peptidase respectively. A hypothesis developed suggested that the cause of the leukodystrophy component in CD was due to release of NAAG by neurons at white matter nodes of Ranvier, its catabolism by astrocytes forming NAA and increased osmotic-hydrostatic pressure as a result of its buildup at these nodes due to the lack of ASPA activity. In this communication, we provide evidence supporting this hypothesis and comment on the cause and possible cure for human CD.

Early Glycine Supplementation Re-Establishes Adrenal Catecholamine Secretion in Hypothalamic Obesity Model in Rats but does not Affect Visceral Adiposity.

Jun 2015 DOI 10.14302/issn.2572-5424.jgm-14-604
Eliza Andreazzi AnaCorresponding author Laboratory of Physiology, Department of Physiology, Federal University of Juiz de Fora, Juiz de Fora/MG - Brazil

Obesity is a worldwide epidemic that features a multifactorial syndrome characterized by a chronic positive energetic unbalance. Neonatal administration of monosodium L-glutamate (MSG) causes lesion on the arcuate nucleus of hypothalamus that led to development of obesity in the adult life in rodents characterized by a notorious accumulation of catecholamine in the adrenal medulla. The amino acid glycine induces catecholamine secretion of adrenal medulla. Thus, the objective of our work was to evaluate the possible effects of glycine administration in the MSG-obesity model in rats and investigate its impact on adrenal catecholamine medulla homeostasis. Male Wistar rats received MSG solution (4mg/g body weight) subcutaneously in the cervical area for 5 days after delivery, controls received saline solution. Animals were also divided in two groups, in which one received tap water added with glycine (0.1g/Kg) after weaning on 21st day until 90 days of life.Biometrical variables, visceral fat pads weight, total content and basal secretion of adrenal cathecolamine were evaluated. Glycine increased Lee index of all tested groups and had no effect on visceral adiposity. However, glycine treatment completely reestablished catecholamine total content and basal secretion of MSG-obese group. In conclusion, although glycine treatment apparently completely reestablishes catecholamine secretion homeostasis it is not sufficient to significant directly reduce visceral adiposity in MSG obesity model in rats.

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