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1

Keighron, Jacqueline D., Yuanmo Wang, and Ann-Sofie Cans. "Electrochemistry of Single-Vesicle Events." Annual Review of Analytical Chemistry 13, no. 1 (2020): 159–81. http://dx.doi.org/10.1146/annurev-anchem-061417-010032.

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Neuronal transmission relies on electrical signals and the transfer of chemical signals from one neuron to another. Chemical messages are transmitted from presynaptic neurons to neighboring neurons through the triggered fusion of neurotransmitter-filled vesicles with the cell plasma membrane. This process, known as exocytosis, involves the rapid release of neurotransmitter solutions that are detected with high affinity by the postsynaptic neuron. The type and number of neurotransmitters released and the frequency of vesicular events govern brain functions such as cognition, decision making, learning, and memory. Therefore, to understand neurotransmitters and neuronal function, analytical tools capable of quantitative and chemically selective detection of neurotransmitters with high spatiotemporal resolution are needed. Electrochemistry offers powerful techniques that are sufficiently rapid to allow for the detection of exocytosis activity and provides quantitative measurements of vesicle neurotransmitter content and neurotransmitter release from individual vesicle events. In this review, we provide an overview of the most commonly used electrochemical methods for monitoring single-vesicle events, including recent developments and what is needed for future research.
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2

Luck, Berkley, Thomas D. Horvath, Kristen A. Engevik, et al. "Neurotransmitter Profiles Are Altered in the Gut and Brain of Mice Mono-Associated with Bifidobacterium dentium." Biomolecules 11, no. 8 (2021): 1091. http://dx.doi.org/10.3390/biom11081091.

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Background: Accumulating evidence indicates that the gut microbiota can synthesize neurotransmitters as well as impact host-derived neurotransmitter levels. In the past, it has been challenging to decipher which microbes influence neurotransmitters due to the complexity of the gut microbiota. Methods: To address whether a single microbe, Bifidobacterium dentium, could regulate important neurotransmitters, we examined Bifidobacteria genomes and explored neurotransmitter pathways in secreted cell-free supernatant using LC-MS/MS. To determine if B. dentium could impact neurotransmitters in vivo, we mono-associated germ-free mice with B. dentium ATCC 27678 and examined fecal and brain neurotransmitter concentrations. Results: We found that B. dentium possessed the enzymatic machinery to generate γ-aminobutyric acid (GABA) from glutamate, glutamine, and succinate. Consistent with the genome analysis, we found that B. dentium secreted GABA in a fully defined microbial media and elevated fecal GABA in B. dentium mono-associated mice compared to germ-free controls. We also examined the tyrosine/dopamine pathway and found that B. dentium could synthesize tyrosine, but could not generate L-dopa, dopamine, norepinephrine, or epinephrine. In vivo, we found that B. dentium mono-associated mice had elevated levels of tyrosine in the feces and brain. Conclusions: These data indicate that B. dentium can contribute to in vivo neurotransmitter regulation.
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Baluta, Sylwia, Dorota Zając, Adam Szyszka, Karol Malecha, and Joanna Cabaj. "Enzymatic Platforms for Sensitive Neurotransmitter Detection." Sensors 20, no. 2 (2020): 423. http://dx.doi.org/10.3390/s20020423.

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A convenient electrochemical sensing pathway was investigated for neurotransmitter detection based on newly synthesized silole derivatives and laccase/horseradish-peroxidase-modified platinum (Pt)/gold (Au) electrodes. The miniature neurotransmitter’s biosensors were designed and constructed via the immobilization of laccase in an electroactive layer of the Pt electrode coated with poly(2,6-bis(3,4-ethylenedioxythiophene)-4-methyl-4-octyl-dithienosilole) and laccase for serotonin (5-HT) detection, and a Au electrode modified with the electroconducting polymer poly(2,6-bis(selenophen-2-yl)-4-methyl-4-octyl-dithienosilole), along with horseradish peroxidase (HRP), for dopamine (DA) monitoring. These sensing arrangements utilized the catalytic oxidation of neurotransmitters to reactive quinone derivatives (the oxidation process was provided in the enzymes’ presence). Under the optimized conditions, the analytical performance demonstrated a convenient degree of sensitivity: 0.0369 and 0.0256 μA mM−1 cm−2, selectivity in a broad linear range (0.1–200) × 10−6 M) with detection limits of ≈48 and ≈73 nM (for the serotonin and dopamine biosensors, respectively). Moreover, the method was successfully applied for neurotransmitter determination in the presence of interfering compounds (ascorbic acid, L-cysteine, and uric acid).
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Anastasaki, Corina, Rasha Barakat, Rui Mu, et al. "CNSC-43. NEUROTRANSMITTER DEPENDENCY UNDERLIES TUMOR GROWTH IN HUMANIZED PEDIATRIC LOW-GRADE GLIOMA MODELS." Neuro-Oncology 26, Supplement_8 (2024): viii50. http://dx.doi.org/10.1093/neuonc/noae165.0199.

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Abstract Brain tumors arise in close association with neurons, suggesting that these non-neoplastic cells may be critical stromal drivers of brain tumor initiation and growth. Previously, we have shown that murine low-grade optic glioma formation and progression in the setting of Neurofibromatosis type 1 (NF1) is dictated by neurons and neuronal activity. In these studies, these neuronal dependencies reflected neuronal activity-driven enzymatic cleavage of a growth factor (neuroligin-3) from oligodendrocyte precursors cells (tumor initiation) or neuronal production of a paracrine factor to stimulate T cell support of optic glioma growth (tumor progression). Since neurons typically communicate with other neurons through neurotransmitters, we sought to explore the possibility that neurotransmitters operate to modulate low-grade glioma growth using humanized mouse models of pilocytic astrocytoma (PA). Leveraging single cell RNA sequencing of three independent sets of pediatric PAs, we identified neurotransmitter pathway enrichment in the tumor cells. This neurotransmitter pathway enrichment reflected aberrant expression of specific neurotransmitter receptors, which we confirmed in three independently generated PA tissue microarrays and in five distinct primary PA cell lines grown in vitro. Moreover, this aberrant neurotransmitter receptor expression established differential neurotransmitter PA growth dependencies in vitro. Importantly, interruption of neurotransmitter signaling in human PA xenografts attenuated tumor growth and ERK activation in Rag1-/- mice in vivo. Finally, we discovered crosstalk between neurotransmitter receptor and receptor tyrosine kinase signaling that revealed another target for therapeutic inhibition. Taken together, these findings elucidate a previously unknown neurotransmitter PA growth dependency amenable to therapeutic targeting.
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Kumar, Ganesh K. "Hypoxia. 3. Hypoxia and neurotransmitter synthesis." American Journal of Physiology-Cell Physiology 300, no. 4 (2011): C743—C751. http://dx.doi.org/10.1152/ajpcell.00019.2011.

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Central and peripheral neurons as well as neuroendocrine cells express a variety of neurotransmitters/modulators that play critical roles in regulation of physiological systems. The synthesis of several neurotransmitters/modulators is regulated by O2-requiring rate-limiting enzymes. Consequently, hypoxia resulting from perturbations in O2 homeostasis can affect neuronal functions by altering neurotransmitter synthesis. Two broad categories of hypoxia are frequently encountered: continuous hypoxia (CH) and intermittent hypoxia (IH). CH is often seen during high altitude sojourns, whereas IH is experienced in sleep-disordered breathing with recurrent apneas (i.e., brief, repetitive cessations of breathing). This article presents what is currently known on the effects of both forms of hypoxia on neurotransmitter levels and neurotransmitter synthesizing enzymes in the central and peripheral nervous systems.
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6

Wang, Ye, Yunyun Zhang, Kai Wang, et al. "Esketamine increases neurotransmitter releases but simplifies neurotransmitter networks in mouse prefrontal cortex." Journal of Neurophysiology 127, no. 2 (2022): 586–95. http://dx.doi.org/10.1152/jn.00462.2021.

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In this study, we found that esketamine significantly increased the cortical concentration of multiple neurotransmitters in mice. However, esketamine dynamically simplified the overall network of cortical neurotransmitters at different behavioral states during the perianesthesia period. The concentration of 5-HT in the medial prefrontal cortex (mPFC) was highly correlated with the esketamine-increased gamma oscillation. These findings suggested that the transformation of the neurotransmitter network rather than the concentrations of neurotransmitters could be more indicative of the consciousness shift during esketamine anesthesia.
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7

Si, Bo, and Edward Song. "Recent Advances in the Detection of Neurotransmitters." Chemosensors 6, no. 1 (2018): 1. http://dx.doi.org/10.3390/chemosensors6010001.

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Neurotransmitters are chemicals that act as messengers in the synaptic transmission process. They are essential for human health and any imbalance in their activities can cause serious mental disorders such as Parkinson’s disease, schizophrenia, and Alzheimer’s disease. Hence, monitoring the concentrations of various neurotransmitters is of great importance in studying and diagnosing such mental illnesses. Recently, many researchers have explored the use of unique materials for developing biosensors for both in vivo and ex vivo neurotransmitter detection. A combination of nanomaterials, polymers, and biomolecules were incorporated to implement such sensor devices. For in vivo detection, electrochemical sensing has been commonly applied, with fast-scan cyclic voltammetry being the most promising technique to date, due to the advantages such as easy miniaturization, simple device architecture, and high sensitivity. However, the main challenges for in vivo electrochemical neurotransmitter sensors are limited target selectivity, large background signal and noise, and device fouling and degradation over time. Therefore, achieving simultaneous detection of multiple neurotransmitters in real time with long-term stability remains the focus of research. The purpose of this review paper is to summarize the recently developed sensing techniques with the focus on neurotransmitters as the target analyte, and to discuss the outlook of simultaneous detection of multiple neurotransmitter species. This paper is organized as follows: firstly, the common materials used for developing neurotransmitter sensors are discussed. Secondly, several sensor surface modification approaches to enhance sensing performance are reviewed. Finally, we discuss recent developments in the simultaneous detection capability of multiple neurotransmitters.
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8

Yao, Yongcheng, Shan Zhao, Yuhong Zhang, et al. "Job-related burnout is associated with brain neurotransmitter levels in Chinese medical workers: a cross-sectional study." Journal of International Medical Research 46, no. 8 (2018): 3226–35. http://dx.doi.org/10.1177/0300060518775003.

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Objective The aim of the present study was to investigate the relationship between job burnout and neurotransmitter levels in medical staff. Methods A total of 80 medical staff were enrolled in the study and assessed for occupational burnout using the Maslach Burnout Inventory – General Survey (MBI-GS). The levels of neurotransmitters in the cerebral cortex were analysed using an SP03 encephalofluctuograph. Results The levels of the neurotransmitters γ-aminobutyric acid, 5-hydroxytryptamine (5-HT), norepinephrine (NE), glutamate, acetylcholine (Achl) and dopamine (DA) were significantly lower in men than in women. Medical staff with lower levels of exhaustion had significantly higher neurotransmitter levels than staff with moderate levels of exhaustion. However, there was no significant interaction between sex and exhaustion on neurotransmitter levels. Canonical correlation showed that exhaustion was positively associated with 5-HT and DA, but negatively associated with NE and Achl, regardless of age and sex. Conclusion Neurotransmitter levels in the cerebral cortex were associated with job-related burnout in medical staff. The findings suggest that long-term job-related burnout may lead to behavioural and psychiatric disorders.
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9

Prado, Vania F., Ashbeel Roy, Benjamin Kolisnyk, Robert Gros, and Marco A. M. Prado. "Regulation of cholinergic activity by the vesicular acetylcholine transporter." Biochemical Journal 450, no. 2 (2013): 265–74. http://dx.doi.org/10.1042/bj20121662.

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Acetylcholine, the first chemical to be identified as a neurotransmitter, is packed in synaptic vesicles by the activity of VAChT (vesicular acetylcholine transporter). A decrease in VAChT expression has been reported in a number of diseases, and this has consequences for the amount of acetylcholine loaded in synaptic vesicles as well as for neurotransmitter release. Several genetically modified mice targeting the VAChT gene have been generated, providing novel models to understand how changes in VAChT affect transmitter release. A surprising finding is that most cholinergic neurons in the brain also can express a second type of vesicular neurotransmitter transporter that allows these neurons to secrete two distinct neurotransmitters. Thus a given neuron can use two neurotransmitters to regulate different physiological functions. In addition, recent data indicate that non-neuronal cells can also express the machinery used to synthesize and release acetylcholine. Some of these cells rely on VAChT to secrete acetylcholine with potential physiological consequences in the periphery. Hence novel functions for the oldest neurotransmitter known are emerging with the potential to provide new targets for the treatment of several pathological conditions.
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10

Yang, Meiqing, Lu Wang, Haozi Lu, and Qizhi Dong. "Advances in MXene-Based Electrochemical (Bio)Sensors for Neurotransmitter Detection." Micromachines 14, no. 5 (2023): 1088. http://dx.doi.org/10.3390/mi14051088.

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Neurotransmitters are chemical messengers that play an important role in the nervous system’s control of the body’s physiological state and behaviour. Abnormal levels of neurotransmitters are closely associated with some mental disorders. Therefore, accurate analysis of neurotransmitters is of great clinical importance. Electrochemical sensors have shown bright application prospects in the detection of neurotransmitters. In recent years, MXene has been increasingly used to prepare electrode materials for fabricating electrochemical neurotransmitter sensors due to its excellent physicochemical properties. This paper systematically introduces the advances in MXene-based electrochemical (bio)sensors for the detection of neurotransmitters (including dopamine, serotonin, epinephrine, norepinephrine, tyrosine, NO, and H2S), with a focus on their strategies for improving the electrochemical properties of MXene-based electrode materials, and provides the current challenges and future prospects for MXene-based electrochemical neurotransmitter sensors.
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11

Doke, Rohit, Ajay Bhagwat, Priyanka Tambe, et al. "Advances in neurotransmitter detection and modulation: Implications for neurological disorders." IP International Journal of Comprehensive and Advanced Pharmacology 9, no. 4 (2024): 236–47. http://dx.doi.org/10.18231/j.ijcaap.2024.035.

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Neurotransmitters are chemicals that amplify, transmit, and transform cellular impulses, facilitating communication across the neurological system. Over the last century, hundreds of these compounds have been identified, with continuous study focussing on their effects on brain health. Neurotransmitters are known to control a variety of processes, including emotions, thoughts, memory, learning, and movement. As a result, abnormalities in neurotransmitter levels have been related to a variety of neurological and neurodegenerative illnesses. This paper seeks to explore the most significant neurotransmitters, categorized into two broad groups: canonical and noncanonical. Additionally, it discusses the connection between these neurotransmitters and key neurological conditions. A concise review of recent advances in neurotransmitter detection methods is also provided, along with insights into how modulating these substances may help restore homeostasis.
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12

Omote, Hiroshi, and Yoshinori Moriyama. "Vesicular Neurotransmitter Transporters: An Approach for Studying Transporters With Purified Proteins." Physiology 28, no. 1 (2013): 39–50. http://dx.doi.org/10.1152/physiol.00033.2012.

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Vesicular storage and subsequent release of neurotransmitters are the key processes of chemical signal transmission. In this process, vesicular neurotransmitter transporters are responsible for loading the signaling molecules. The use of a “clean biochemical” approach with purified, recombinant transporters has helped in the identification of novel vesicular neurotransmitter transporters and in the analysis of the control of signal transmission.
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13

Jung-Klawitter, Sabine, and Oya Kuseyri Hübschmann. "Analysis of Catecholamines and Pterins in Inborn Errors of Monoamine Neurotransmitter Metabolism—From Past to Future." Cells 8, no. 8 (2019): 867. http://dx.doi.org/10.3390/cells8080867.

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Inborn errors of monoamine neurotransmitter biosynthesis and degradation belong to the rare inborn errors of metabolism. They are caused by monogenic variants in the genes encoding the proteins involved in (1) neurotransmitter biosynthesis (like tyrosine hydroxylase (TH) and aromatic amino acid decarboxylase (AADC)), (2) in tetrahydrobiopterin (BH4) cofactor biosynthesis (GTP cyclohydrolase 1 (GTPCH), 6-pyruvoyl-tetrahydropterin synthase (PTPS), sepiapterin reductase (SPR)) and recycling (pterin-4a-carbinolamine dehydratase (PCD), dihydropteridine reductase (DHPR)), or (3) in co-chaperones (DNAJC12). Clinically, they present early during childhood with a lack of monoamine neurotransmitters, especially dopamine and its products norepinephrine and epinephrine. Classical symptoms include autonomous dysregulations, hypotonia, movement disorders, and developmental delay. Therapy is predominantly based on supplementation of missing cofactors or neurotransmitter precursors. However, diagnosis is difficult and is predominantly based on quantitative detection of neurotransmitters, cofactors, and precursors in cerebrospinal fluid (CSF), urine, and blood. This review aims at summarizing the diverse analytical tools routinely used for diagnosis to determine quantitatively the amounts of neurotransmitters and cofactors in the different types of samples used to identify patients suffering from these rare diseases.
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Lussier, Félix, Thibault Brulé, Marie-Josée Bourque, Charles Ducrot, Louis-Éric Trudeau, and Jean-François Masson. "Dynamic SERS nanosensor for neurotransmitter sensing near neurons." Faraday Discussions 205 (2017): 387–407. http://dx.doi.org/10.1039/c7fd00131b.

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Current electrophysiology and electrochemistry techniques have provided unprecedented understanding of neuronal activity. However, these techniques are suited to a small, albeit important, panel of neurotransmitters such as glutamate, GABA and dopamine, and these constitute only a subset of the broader range of neurotransmitters involved in brain chemistry. Surface-enhanced Raman scattering (SERS) provides a unique opportunity to detect a broader range of neurotransmitters in close proximity to neurons. Dynamic SERS (D-SERS) nanosensors based on patch-clamp-like nanopipettes decorated with gold nanoraspberries can be located accurately under a microscope using techniques analogous to those used in current electrophysiology or electrochemistry experiments. In this manuscript, we demonstrate that D-SERS can measure in a single experiment ATP, glutamate (glu), acetylcholine (ACh), GABA and dopamine (DA), among other neurotransmitters, with the potential for detecting a greater number of neurotransmitters. The SERS spectra of these neurotransmitters were identified with a barcoding data processing method and time series of the neurotransmitter levels were constructed. The D-SERS nanosensor was then located near cultured mouse dopaminergic neurons. The detection of neurotransmitters was performed in response to a series of K<sup>+</sup>depolarisations, and allowed the detection of elevated levels of both ATP and dopamine. Control experiments were also performed near glial cells, showing only very low basal detection neurotransmitter events. This paper demonstrates the potential of D-SERS to detect neurotransmitter secretion events near living neurons, but also constitutes a strong proof-of-concept for the broad application of SERS to the detection of secretion events by neurons or other cell types in order to study normal or pathological cell functions.
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Harris, Keith D., Meital Weiss, and Amotz Zahavi. "Why are neurotransmitters neurotoxic? An evolutionary perspective." F1000Research 3 (December 2, 2014): 179. http://dx.doi.org/10.12688/f1000research.4828.2.

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In the CNS, minor changes in the concentration of neurotransmitters such as glutamate or dopamine can lead to neurodegenerative diseases. We present an evolutionary perspective on the function of neurotransmitter toxicity in the CNS. We hypothesize that neurotransmitters are selected because of their toxicity, which serves as a test of neuron quality and facilitates the selection of neuronal pathways. This perspective may offer additional explanations for the reduction of neurotransmitter concentration in the CNS with age, and suggest an additional role for the blood-brain barrier. It may also suggest a connection between the specific toxicity of the neurotransmitters released in a specific region of the CNS, and elucidate their role as chemicals that are optimal for testing the quality of cells in that region.
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16

van Karnebeek, Clara D. M., Mary Dunbar, Csilla Egri, et al. "Secondary Abnormal CSF Neurotransmitter Metabolite Profiles in a Pediatric Tertiary Care Centre." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 45, no. 2 (2017): 206–13. http://dx.doi.org/10.1017/cjn.2017.271.

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AbstractBackground:Secondary neurotransmitter deficiencies have been reported in several reviews. Our primary aim was to assess the relationship among epilepsy, antiseizure medications, and specific neurotransmitter abnormalities. We also evaluated movement disorders and brain abnormalities via magnetic resonance imaging scans in patients with secondary neurotransmitter defects.Methods:This is a retrospective case series of 376 patients who underwent neurotransmitter analysis at BC Children’s Hospital between 2009 and 2013, for a variety of neurological presentations. The biochemical genetics laboratory database was interrogated for results of cerebrospinal fluid neurotransmitter analyses. Clinical data for patients with abnormal results were collected from the hospital charts. Statistical analysis included one-way analysis of variance, chi-square, and a two-way contingency table.Results:Abnormal neurotransmitter values were identified in 67 (17.8%) patients, two (0.53%) of which were attributable to a congenital neurotransmitter disorder and 11 (16.9%) secondary to other genetic diagnoses. Of 64 patients with secondary abnormal neurotransmitter values, 38 (59%) presented with epilepsy and 20 (31%) with movement disorders. A combination of epilepsy and movement disorder was less frequent.Discussion:Acknowledging the limitations of this retrospective chart review, we conclude that, in our cohort, in addition to patients with movement disorders, a considerable number of patients with epilepsy and epileptic encephalopathy also showed secondary neurotransmitter mono-amine abnormalities. There is no clear relation, however, between clinical phenotype and type of neurotransmitter affected. In addition, no association was identified between the type of antiseizure medications and affected neurotransmitter type. We outline the need for prospective studies to further enrich our understanding of the relation between epilepsy and neurotransmitters with a focus on improving treatments and patient outcomes.
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Court, Jenny A., and Elaine K. Perry. "Neurotransmitter Abnormalities in Vascular Dementia." International Psychogeriatrics 15, S1 (2003): 81–87. http://dx.doi.org/10.1017/s1041610203009013.

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A number of neurotransmitters, including acetylcholine, serotonin, noradrenaline, and dopamine, modulate cerebral perfusion. In vascular dementia, reductions in markers of cholinergic innervation are consistently reported, and there are some indications that the serotonergic and dopaminergic systems may also be affected. Limited data indicate that the numbers of nucleus basalis, locus coeruleus, and dorsal raphé neurons and the density of neurotransmitter receptors are not reduced in the majority of cases. These data suggest neurotransmitter systems as a potential therapeutic target in vascular dementia.
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Bertuzzi, Maria, Weipang Chang, and Konstantinos Ampatzis. "Adult spinal motoneurons change their neurotransmitter phenotype to control locomotion." Proceedings of the National Academy of Sciences 115, no. 42 (2018): E9926—E9933. http://dx.doi.org/10.1073/pnas.1809050115.

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A particularly essential determinant of a neuron’s functionality is its neurotransmitter phenotype. While the prevailing view is that neurotransmitter phenotypes are fixed and determined early during development, a growing body of evidence suggests that neurons retain the ability to switch between different neurotransmitters. However, such changes are considered unlikely in motoneurons due to their crucial functional role in animals’ behavior. Here we describe the expression and dynamics of glutamatergic neurotransmission in the adult zebrafish spinal motoneuron circuit assembly. We demonstrate that part of the fast motoneurons retain the ability to switch their neurotransmitter phenotype under physiological (exercise/training) and pathophysiological (spinal cord injury) conditions to corelease glutamate in the neuromuscular junctions to enhance animals’ motor output. Our findings suggest that motoneuron neurotransmitter switching is an important plasticity-bestowing mechanism in the reconfiguration of spinal circuits that control movements.
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Salim, Agus, Nyoman Suwarta, and Arifin Mado. "STUDY LITERATURE: BIOPSYCHOLOGICAL REVIEW IN IMPROVING CHILDREN'S CONCENTRATION." Academic Journal Research 2, no. 1 (2024): 72–88. http://dx.doi.org/10.61796/acjoure.v2i1.120.

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Concentration is very important and needed for children in following the learning process. learning concentration can be seen from an increase in the presence of neurotransmitters. Neurotransmitters function as chemical messengers that play an important role in information processing throughout the nervous system. The purpose of this research is to describe the Literature Study: A Biopsychological Review in Improving Children's Concentration. This research uses library research with a qualitative descriptive approach. Based on the results of the review of 25 (twenty-five) journals examined by the author, there are various effectiveness of neurotransmitter performance involved in various brain functions, such as sleep, mood, emotion, attention, and learning and memory. The conclusions of this study include: 1) Neurotransmitter metabolites include biogenic amines (catecholamines norepinephrine, epinephrine, and dopamine and serotonin) and amino acids (glycine, glutamate, and γ-aminobutyric acid [GABA]), 2) Serotonin is useful for neurotransmitters and concentration, 3) Neurotransmitters including acetylcholine play an important role in the development of brain nerve structures and cells. Acetylcholine (ACh) is the first identified cholinergic neurotransmitter, and changes in its content can fully reflect the growth and development of the body as well as learning ability and memory, 4) Students who are able to concentrate during lessons will have higher memory and easily understand what is learned and 5) The researcher suggests that future studies examine the effect of one of the various types of neurotransmitters on children's concentration and motivation to learn.
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Choi, Hye Kyu, Jin-Ha Choi, and Jinho Yoon. "An Updated Review on Electrochemical Nanobiosensors for Neurotransmitter Detection." Biosensors 13, no. 9 (2023): 892. http://dx.doi.org/10.3390/bios13090892.

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Neurotransmitters are chemical compounds released by nerve cells, including neurons, astrocytes, and oligodendrocytes, that play an essential role in the transmission of signals in living organisms, particularly in the central nervous system, and they also perform roles in realizing the function and maintaining the state of each organ in the body. The dysregulation of neurotransmitters can cause neurological disorders. This highlights the significance of precise neurotransmitter monitoring to allow early diagnosis and treatment. This review provides a complete multidisciplinary examination of electrochemical biosensors integrating nanomaterials and nanotechnologies in order to achieve the accurate detection and monitoring of neurotransmitters. We introduce extensively researched neurotransmitters and their respective functions in biological beings. Subsequently, electrochemical biosensors are classified based on methodologies employed for direct detection, encompassing the recently documented cell-based electrochemical monitoring systems. These methods involve the detection of neurotransmitters in neuronal cells in vitro, the identification of neurotransmitters emitted by stem cells, and the in vivo monitoring of neurotransmitters. The incorporation of nanomaterials and nanotechnologies into electrochemical biosensors has the potential to assist in the timely detection and management of neurological disorders. This study provides significant insights for researchers and clinicians regarding precise neurotransmitter monitoring and its implications regarding numerous biological applications.
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Stern, Peter R. "Daylight Determines Dopamine." Science Signaling 6, no. 273 (2013): ec95-ec95. http://dx.doi.org/10.1126/scisignal.2004276.

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Expression of the appropriate neurotransmitters is essential for the function of neural circuits. Can neurons change their transmitter phenotype to deal with alterations in the environment? Dulcis et al. (see the Perspective by Birren and Marder) exposed adult rats to different photoperiods mimicking summer and winter daylengths. Neurotransmitter expression switched between dopamine and somatostatin in hypothalamic neurons that regulate release of corticotropin-releasing factor. Transmitter switching occurred at the transcriptional level and was accompanied by changes in postsynaptic receptors.D. Dulcis, P. Jamshidi, S. Leutgeb, N. C. Spitzer, Neurotransmitter switching in the adult brain regulates behavior. Science340, 449–453 (2013). [Abstract][Full Text]S. J. Birren, E. Marder, Plasticity in the neurotransmitter repertoire. Science340, 436–437 (2013). [Abstract][Full Text]
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Lachance, Gabriel Philippe, Dominic Gauvreau, Élodie Boisselier, Mounir Boukadoum, and Amine Miled. "Breaking Barriers: Exploring Neurotransmitters through In Vivo vs. In Vitro Rivalry." Sensors 24, no. 2 (2024): 647. http://dx.doi.org/10.3390/s24020647.

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Neurotransmitter analysis plays a pivotal role in diagnosing and managing neurodegenerative diseases, often characterized by disturbances in neurotransmitter systems. However, prevailing methods for quantifying neurotransmitters involve invasive procedures or require bulky imaging equipment, therefore restricting accessibility and posing potential risks to patients. The innovation of compact, in vivo instruments for neurotransmission analysis holds the potential to reshape disease management. This innovation can facilitate non-invasive and uninterrupted monitoring of neurotransmitter levels and their activity. Recent strides in microfabrication have led to the emergence of diminutive instruments that also find applicability in in vitro investigations. By harnessing the synergistic potential of microfluidics, micro-optics, and microelectronics, this nascent realm of research holds substantial promise. This review offers an overarching view of the current neurotransmitter sensing techniques, the advances towards in vitro microsensors tailored for monitoring neurotransmission, and the state-of-the-art fabrication techniques that can be used to fabricate those microsensors.
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Brennenstuhl, Heiko, Sabine Jung-Klawitter, Birgit Assmann, and Thomas Opladen. "Inherited Disorders of Neurotransmitters: Classification and Practical Approaches for Diagnosis and Treatment." Neuropediatrics 50, no. 01 (2018): 002–14. http://dx.doi.org/10.1055/s-0038-1673630.

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AbstractNeurotransmitter deficiencies are rare neurological disorders with clinical onset during childhood. The disorders are caused by genetic defects in the enzymes involved in synthesis, degradation, or transport of neurotransmitters or by defects in the cofactor biosynthesis such as tetrahydrobiopterin (BH4). With the newly described DNAJC12 deficiency, a chaperon-associated neurotransmitter disorder, the pathophysiological spectrum has been broadened. All deficiencies result in a lack of monoamine neurotransmitters, especially dopamine and its products, with a subset leading to decreased levels of serotonin. Symptoms can occur already in the neonatal period. Classical signs are hypotonia, movement disorders, autonomous dysregulations, and impaired development. Diagnosis depends on quantitative detection of neurotransmitters in cerebrospinal fluid, since peripheral markers in blood or urine are less reliable. Treatment is based on supplementation of the missing neurotransmitter precursors or restoring deficient cofactors for endogenous enzymatic synthesis. In recent years, knowledge about this orphan group of diseases increased substantially among clinicians. However, the difficult task of integrating clinical symptoms and laboratory values still leads to a critical delay in diagnosis and therapy for patients. This review aims at enhancing the understanding of neurotransmitter disorders and should help practicing clinicians to choose useful diagnostic steps on the way to a valid diagnosis.
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Joseph, Litty, Saneha O.R, and Chinchu Ravi. "Insomnia: Therapy and Role of neurotransmitters." Journal of University of Shanghai for Science and Technology 23, no. 12 (2021): 511–24. http://dx.doi.org/10.51201/jusst/21/121052.

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Insomnia is one of the most common sleep disorders which affects 30-40 percent of the adult population. The present article provides a combined review on prevalence, categories of insomnia, pathophysiology, role of neurotransmitter on sleep and different types of therapies for insomnia. From this review it was estimated that hormones like melatonin, cortisol, and others produced by the hypothalamic-pituitary-adrenal axis regulate the sleep-wake cycle. Disturbance of this cycle leads to insomnia. Furthermore, Neurotransmitter like GABA-Lglutamic acid, Acetylcholine, Norepinephrine, Dopamine, Serotonin, Steroids, Orexin, and Adenosine plays a major role in sleep regulation. Any alteration or disturbance in the neurotransmitter level affects sleep. It was concluded that Mechanism of action of almost all natural and synthetic derived drugs in regulation of neurotransmitters.
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Devaraj, Uthirakumar. "Glutamate Elicits Therapeutic Responses in Light-Induced Sleep-Deprived Zebrafish, Danio rerio." Bioscience Biotechnology Research Communications 14, no. 4 (2021): 1577–83. http://dx.doi.org/10.21786/bbrc/14.4.32.

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Sleep deprivation disrupts most neurotransmitters, which can lead to adverse behavioural changes and other psychiatric illnesses. Many neurotransmitter systems, including dopamine (DA), serotonin (5-HT), norepinephrine (N.E.) and GABA, have been implicated in the pathophysiology of mood disorders. The precise significance of sleep deprivation (S.D.) changes in the neurotransmitter levels and the mechanism underlying behavioural alterations is unknown. According to research, sleep deprivation (S.D.) has a major effect on an individual’s quality of life and ability to perform essential physiological functions. As a result, we wanted to confirm the levels of neurotransmitters and behavioural modifications in zebrafish after 24, 48, and 72 hours of sleep deprivation and glutamate treatment on the sleep-deprived groups. The T-maze test was used to assess learning and memory alterations in zebrafish. We used the Novel Tank Test (NTT) and Light and Dark Test (LDT) to examine the anxiety-like behaviour. The spectrofluorimetric method was used to determine the quantities of DA, 5-HT, N.E. and GABA. From this study, it is evident that 72h sleep-deprived fish had a loss of learning and memory via T-maze test and also the anxiety levels were very high in the sleep-deprived group than the other groups. The groups that received glutamate after sleep deprivation showed betterment in the behavioural response. Also, the levels of neurotransmitters were increased in the glutamate treated groups than the sleep-deprived groups. Our findings indicate that sleep loss dramatically impairs behavioural responses and disrupts most neurotransmitter concentrations. When sleep-deprived fish were given glutamate, their behaviour and neurotransmitter levels were nearly identical to those of the control group. This study will have a greater impact on sleep deprivation therapy and pave the way for using the neurotransmitters as external therapeutic agents in treating sleep deprivation and other behavioural changes related to sleep deprivation.It has been suggested that zebrafish is an excellent testing subject for loss of sleep on cognition and that it may also be an efficient model for unravelling the pathways that underpin learning and memory formation.
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Kim, Dongshin, and Jang-Sik Lee. "Emulating Excitatory and Inhibitory Functions in Artificial Synaptic Devices." ECS Meeting Abstracts MA2022-02, no. 33 (2022): 2585. http://dx.doi.org/10.1149/ma2022-02332585mtgabs.

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Synaptic signals are controlled by neurotransmitters. The synaptic signals can be excited or inhibited depending on the types of neurotransmitters. The demonstration of the balancing between excitatory and inhibitory signals has important implications for the complex and efficient computing of the nervous system. Emulating the excitatory-inhibitory balancing behaviors of the nervous system is one way to establish neuromorphic computing. In this study, we demonstrate artificial synapses using PEDOT:PSS channel and neurotransmitter solutions to emulate the excitatory-inhibitory balancing behaviors. The devices show excitatory and inhibitory postsynaptic characteristics using the neurotransmitter solutions. Also, using the interaction between excitatory and inhibitory synaptic responses, the devices emulate the excitatory-inhibitory balancing behaviors of the nervous system. The devices exhibit multifunctional characteristics similar to the biological synapses, resulting in their potential for use in neuromorphic devices.
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Ferré, Sergi, Francisco Ciruela, César Quiroz, et al. "Adenosine Receptor Heteromers and their Integrative Role in Striatal Function." Scientific World JOURNAL 7 (2007): 74–85. http://dx.doi.org/10.1100/tsw.2007.211.

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By analyzing the functional role of adenosine receptor heteromers, we review a series of new concepts that should modify our classical views of neurotransmission in the central nervous system (CNS). Neurotransmitter receptors cannot be considered as single functional units anymore. Heteromerization of neurotransmitter receptors confers functional entities that possess different biochemical characteristics with respect to the individual components of the heteromer. Some of these characteristics can be used as a “biochemical fingerprint” to identify neurotransmitter receptor heteromers in the CNS. This is exemplified by changes in binding characteristics that are dependent on coactivation of the receptor units of different adenosine receptor heteromers. Neurotransmitter receptor heteromers can act as “processors” of computations that modulate cell signaling, sometimes critically involved in the control of pre- and postsynaptic neurotransmission. For instance, the adenosine A1-A2Areceptor heteromer acts as a concentration-dependent switch that controls striatal glutamatergic neurotransmission. Neurotransmitter receptor heteromers play a particularly important integrative role in the “local module” (the minimal portion of one or more neurons and/or one or more glial cells that operates as an independent integrative unit), where they act as processors mediating computations that convey information from diverse volume-transmitted signals. For instance, the adenosine A2A-dopamine D2receptor heteromers work as integrators of two different neurotransmitters in the striatal spine module.
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28

Weishaupt, Ann-Kathrin, Laura Kubens, Lysann Ruecker, Tanja Schwerdtle, Michael Aschner, and Julia Bornhorst. "A Reliable Method Based on Liquid Chromatography–Tandem Mass Spectrometry for the Simultaneous Quantification of Neurotransmitters in Caenorhabditis elegans." Molecules 28, no. 14 (2023): 5373. http://dx.doi.org/10.3390/molecules28145373.

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Neurotransmitters like dopamine (DA), serotonin (SRT), γ-aminobutyric acid (GABA) and acetylcholine (ACh) are messenger molecules that play a pivotal role in transmitting excitation between neurons across chemical synapses, thus enabling complex processes in the central nervous system (CNS). Balance in neurotransmitter homeostasis is essential, and altered neurotransmitter levels are associated with various neurological disorders, e.g., loss of dopaminergic neurons (Parkinson’s disease) or altered ACh synthesis (Alzheimer’s disease). Therefore, it is crucial to possess adequate tools to assess precise neurotransmitter levels, and to apply targeted therapies. An established in vivo model to study neurotoxicity is the model organism Caenorhabditis elegans (C. elegans), as its neurons have been well characterized and functionally are analogous to mammals. We have developed a liquid chromatography–tandem mass spectrometry (LC-MS/MS) method including a sample preparation assuring neurotransmitter stability, which allows a simultaneous neurotransmitter quantification of DA, SRT, GABA and ACh in C. elegans, but can easily be applied to other matrices. LC-MS/MS combined with isotope-labeled standards is the tool of choice, due to its otherwise unattainable sensitivity and specificity. Using C. elegans together with our analytically validated and verified method provides a powerful tool to evaluate mechanisms of neurotoxicity, and furthermore to identify possible therapeutic approaches.
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Ayala‐Lopez, Nadia, and Stephanie W. Watts. "Physiology and Pharmacology of Neurotransmitter Transporters." Comprehensive Physiology 11, no. 3 (2021): 2279–95. https://doi.org/10.1002/j.2040-4603.2021.tb00180.x.

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AbstractRegulation of the ability of a neurotransmitter [our focus: serotonin, norepinephrine, dopamine, acetylcholine, glycine, and gamma‐aminobutyric acid (GABA)] to reach its receptor targets is regulated in part by controlling the access the neurotransmitter has to receptors. Transporters, located at both the cellular plasma membrane and in subcellular vesicles, carry a myriad of responsibilities that include enabling neurotransmitter release and controlling uptake of neurotransmitter back into a cell or vesicle. Driven largely by electrochemical gradients, these transporters move neurotransmitters. The regulation of the transporters themselves through changes in expression and/or posttranslational modification allows for fine‐tuning of this system. Transporters have been best recognized as targets for psychoactive stimulants and remain a mainstay target of primarily central nervous system (CNS) acting drugs for treatment of debilitating diseases such as depression and anxiety. Studies reveal, however, that transporters are found and functional in tissues outside the CNS (gastrointestinal and cardiovascular tissues, for example). The importance of neurotransmitter transporters is underscored with discoveries that dysfunction of transporters can cause life‐changing disease. This article provides a high‐level review of major classes of both plasma membrane transporters and vesicular transporters. © 2021 American Physiological Society. Compr Physiol 11:2279‐2295, 2021.
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Volkova, Alla Andreevna, Roman Anatolievich Kalekin, Alevtina Mikhailovna Orlova, Albina Zakharovna Pavlova, Olga Genrikhovna Astashkina, and Andrey Leonidovich Pavlov. "The effect of zaleplon on metabolic changes in neurotransmitters and toxic effects in Danio fish." Toxicological Review 31, no. 3 (2023): 192–203. http://dx.doi.org/10.47470/0869-7922-2023-31-3-192-203.

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Introduction. Z-drugs are a group of “non-benzodiazepine” drugs with the main mode of action regulating sleep behavior in humans through exposure to GABA receptors. There are reports indicating the toxic effects of overdose and abuse of zaleplon. However, information on the effect of Z-drugs on neurotransmitter levels is scarce. &#x0D; The aim of this study was to study the effect of zaleplon exposure on neurotransmitter levels in the larvae of Danio fish using targeted metabolomics. &#x0D; Material and methods. 4-hour exposure to zaleplon in concentrations of 0.1, 1.0, 10, 100 and 1000 μg/l was carried out on the larvae of Danio fish. Intervention groups were compared with control groups. Each group consisted of 20 larvae of Danio fish. Neurotransmitters and their metabolites were measured using high-performance liquid chromatography combined with tandem mass spectrometry (HPLC-MS/MS). &#x0D; Results. Twenty-two metabolites associated with neurotransmission were quantified. Significantly increased metabolites were tryptophan, serotonin, 5-hydroxyindolacetic acid, acetylserotonin, epinephrine and choline. Significantly reduced metabolites were 5-hydroxytryptophan, 5-methoxytryptamine, dopamine, normetanephrine, metanephrine, kynurenine, 3-hydroxykinurenine, anthranilic acid and gamma-aminobutyric acid.&#x0D; Limitation. When studying metabolic changes in neurotransmitters and toxic effects in Danio fish, the results of a group of 20 larvae were analyzed, which is a sufficient sample to state the results obtained.&#x0D; Conclusion. Exposure to zaleplon caused metabolic changes in the concentrations of neurotransmitters associated with most major neurotransmitter systems.
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Zestos, Alexander George, Pauline Wonnenberg, Victoria Connaughton, and Kyle Laurie. "(Invited) Co-Detection of Dopamine and Metabolites Using Fast Scan Cyclic Voltammetry and Modified Carbon Fiber-Microelectrodes." ECS Meeting Abstracts MA2019-02, no. 55 (2019): 2424. http://dx.doi.org/10.1149/ma2019-02/55/2424.

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Fast scan cyclic voltammetry (FSCV) and carbon-fiber microelectrodes (CFMEs) have been utilized used to detect several important neurochemicals in vivo. However, this method is limited due to the ability to discriminate dopamine from several of its metabolites. Carbon nanotube and polymer modified microelectrodes will be utilized to detect physiologically low levels of neurotransmitters that also resist surface fouling and have high temporal resolution to detect fast changes of neurotransmitters. Furthermore, novel electrode coatings and waveforms will also be utilized to detect several neurotransmitter metabolites such as dopamine, norepinephrine, normetanephrine, 3-methoxytyramine (3-MT), homovanillic acid (HVA), 3,4 dihydroxyphenylacetic acid (DOPAC), and other metabolites. Currently, dopamine is thought to be an important neurotransmitter concerning several disease states such Parkinson’s disease, drug abuse (amphetamine, cocaine, etc.), and even for gambling and sex-disorders. However, dopamine is metabolized on a subsecond timescale, and studies have pointed to the importance of neurotransmitter metabolites in these disease states apart from dopamine. Presently, there is no method to selectively co-detect these neurotransmitter metabolites of dopamine utilizing FSCV. Through several waveform modifications and polymer electrode coatings, we develop a novel method to tune the detection of dopamine and said metabolites, which will help differentiate dopamine and respective metabolites through the shapes and positions of their respective cyclic voltammograms. Preliminary measurements have also been made in zebrafish whole brain ex vivo showing the application of this technique in biological tissue. Discriminating the detection of dopamine from its metabolites will have many implications in better understanding complex disease, behavioral, and pharmacological states.
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32

Chandana, Bandaru, G. Krishna Mohan, and M. Sandhya Rani. "Advanced Molecular Mechanisms of Epilepsy." Journal of Pharmaceutical Quality Assurance and Quality Control 5, no. 2 (2023): 22–34. http://dx.doi.org/10.46610/jqaqc.2023.v05i02.004.

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The Central Nervous System (CNS) is a complex network composed of the cerebral cortex and the vertebral column, orchestrating intricate processes through neural networks and chemical regulation. Neurotransmission in the CNS involves neurotransmitters, neuromodulators, neuromediators, and neurotropic factors, playing distinct roles in cellular activity and synaptic plasticity. Various neurotransmitters such as dopamine, glutamate, GABA, glycine, serotonin, and others exert diverse effects on the CNS through specific receptors, influencing synaptic transmission and neuronal excitability. GABA, the primary inhibitory neurotransmitter, acts via GABA-A and GABA-B receptors, modulating Cl-ion channels and second messenger systems, impacting seizure activity and CNS function. Epilepsy, a neurological disorder characterized by abnormal brain activity leading to recurrent seizures, results from an imbalance between excitatory (glutamate) and inhibitory (GABA) systems. The pathophysiology involves neuronal hyperexcitability, disrupted ion channels, and neurotransmitter imbalances, leading to seizures with varying symptoms and severity. The etiology of epilepsy encompasses genetic predisposition, head injuries, brain disorders, infections, prenatal injuries, and developmental disorders. Treatment options include medications, surgery, brain stimulation therapies, and dietary interventions like the ketogenic diet Understanding the mechanisms underlying epilepsy involves exploring neurotransmitter interactions, ion channel dynamics, and neuroendocrine modulation. Neuropeptide Y (NPY) and steroid hormones, such as testosterone and estrogen, play roles in seizure susceptibility, offering potential avenues for therapeutic intervention. In conclusion, unravelling the complexities of the CNS and epilepsy involves deciphering intricate neural pathways, neurotransmitter functions, and hormonal influences. Developing targeted therapies that modulate these intricate systems may offer promising approaches for managing epilepsy and related neurological conditions.
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33

Nelson, N., and H. Lill. "Porters and neurotransmitter transporters." Journal of Experimental Biology 196, no. 1 (1994): 213–28. http://dx.doi.org/10.1242/jeb.196.1.213.

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Uptake of neurotransmitters involves multiple transporters acting in different brain locations under different physiological conditions. The vesicular transporters are driven by a proton-motive force generated by a V-ATPase and their substrates are taken up via proton/substrate exchange. The plasma membrane transporters are driven by an electrochemical gradient of sodium generated by a Na+/K(+)-ATPase. Two distinct families of transporters were identified in this group. One cotransports sodium with glutamate and other amino acids and requires additionally an outwardly directed potassium gradient. The second cotransports sodium, chloride and a variety of neurotransmitters, including gamma-aminobutyric acid (GABA), glycine and monoamines. Genes and cDNA encoding several members of the latter family have been cloned and studied in detail. The structure and function as well as the evolutionary relationships among these neurotransmitter transporters are discussed.
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34

Gros, Mónica, Belén Gros, José Emilio Mesonero, and Eva Latorre. "Neurotransmitter Dysfunction in Irritable Bowel Syndrome: Emerging Approaches for Management." Journal of Clinical Medicine 10, no. 15 (2021): 3429. http://dx.doi.org/10.3390/jcm10153429.

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Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder whose aetiology is still unknown. Most hypotheses point out the gut-brain axis as a key factor for IBS. The axis is composed of different anatomic and functional structures intercommunicated through neurotransmitters. However, the implications of key neurotransmitters such as norepinephrine, serotonin, glutamate, GABA or acetylcholine in IBS are poorly studied. The aim of this review is to evaluate the current evidence about neurotransmitter dysfunction in IBS and explore the potential therapeutic approaches. IBS patients with altered colorectal motility show augmented norepinephrine and acetylcholine levels in plasma and an increased sensitivity of central serotonin receptors. A decrease of colonic mucosal serotonin transporter and a downregulation of α2 adrenoceptors are also correlated with visceral hypersensitivity and an increase of 5-hydroxyindole acetic acid levels, enhanced expression of high affinity choline transporter and lower levels of GABA. Given these neurotransmitter dysfunctions, novel pharmacological approaches such as 5-HT3 receptor antagonists and 5-HT4 receptor agonists are being explored for IBS management, for their antiemetic and prokinetic effects. GABA-analogous medications are being considered to reduce visceral pain. Moreover, agonists and antagonists of muscarinic receptors are under clinical trials. Targeting neurotransmitter dysfunction could provide promising new approaches for IBS management.
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35

Zestos, Alexander G. "Carbon Nanoelectrodes for the Electrochemical Detection of Neurotransmitters." International Journal of Electrochemistry 2018 (August 1, 2018): 1–19. http://dx.doi.org/10.1155/2018/3679627.

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Carbon-based electrodes have been developed for the detection of neurotransmitters over the past 30 years using voltammetry and amperometry. The traditional electrode for neurotransmitter detection is the carbon fiber microelectrode (CFME). The carbon-based electrode is suitable for in vivo neurotransmitter detection due to the fact that it is biocompatible and relatively small in surface area. The advent of nanoscale electrodes is in high demand due to smaller surface areas required to target specific brain regions that are also minimally invasive and cause relatively low tissue damage when implanted into living organisms. Carbon nanotubes (CNTs), carbon nanofibers, carbon nanospikes, and carbon nanopetals among others have all been utilized for this purpose. Novel electrode materials have also required novel insulations such as glass, epoxy, and polyimide coated fused silica capillaries for their construction and usage. Recent research developments have yielded a wide array of carbon nanoelectrodes with superior properties and performances in comparison to traditional electrode materials. These electrodes have thoroughly enhanced neurotransmitter detection allowing for the sensing of biological compounds at lower limits of detection, fast temporal resolution, and without surface fouling. This will allow for greater understanding of several neurological disease states based on the detection of neurotransmitters.
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36

Bamicha, Victoria, Pantelis Pergantis, Charalabos Skianis, and Athanasios Drigas. "Computational Neuroscience’s Influence on Autism Neuro-Transmission Research: Mapping Serotonin, Dopamine, Gaba, and Glutamate." Biomedicines 13, no. 6 (2025): 1420. https://doi.org/10.3390/biomedicines13061420.

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Autism spectrum disorder is a complex and diverse neurobiological condition. Understanding the mechanisms and causes of the disorder requires an in-depth study and modeling of the immune, mitochondrial, and neurological systems. Computational neuroscience enhances psychiatric science by employing machine learning techniques on neural networks, combining data on brain activity with the pathophysiological and biological characteristics of psychiatric–neurobiological disorders. The research explores the integration of neurotransmitter activity into computational models and their potential roles in diagnosing and treating autism using computational methods. This research employs a narrative review that focuses on four neurotransmitter systems directly related to the manifestation of autism, specifically the following neurotransmitters: serotonin, dopamine, glutamate, and gamma-aminobutyric acid (GABA). This study reveals that computational neuroscience advances autism diagnosis and treatment by identifying genetic factors and improving the efficiency of diagnosis. Neurotransmitters play a crucial role in the function of brain cells, enhancing synaptic conduction and signal transmission. However, the interaction of chemical compounds with genetic factors and network alterations influences the pathophysiology of autism. This study integrates the investigation of computational approaches in four neurotransmitter systems associated with ASD. It improves our understanding of the disorder and provides insights that could stimulate further research, thereby contributing to the development of effective treatments.
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37

Krishna, Gokul, Joshua A. Beitchman, Caitlin E. Bromberg, and Theresa Currier Thomas. "Approaches to Monitor Circuit Disruption after Traumatic Brain Injury: Frontiers in Preclinical Research." International Journal of Molecular Sciences 21, no. 2 (2020): 588. http://dx.doi.org/10.3390/ijms21020588.

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Mild traumatic brain injury (TBI) often results in pathophysiological damage that can manifest as both acute and chronic neurological deficits. In an attempt to repair and reconnect disrupted circuits to compensate for loss of afferent and efferent connections, maladaptive circuitry is created and contributes to neurological deficits, including post-concussive symptoms. The TBI-induced pathology physically and metabolically changes the structure and function of neurons associated with behaviorally relevant circuit function. Complex neurological processing is governed, in part, by circuitry mediated by primary and modulatory neurotransmitter systems, where signaling is disrupted acutely and chronically after injury, and therefore serves as a primary target for treatment. Monitoring of neurotransmitter signaling in experimental models with technology empowered with improved temporal and spatial resolution is capable of recording in vivo extracellular neurotransmitter signaling in behaviorally relevant circuits. Here, we review preclinical evidence in TBI literature that implicates the role of neurotransmitter changes mediating circuit function that contributes to neurological deficits in the post-acute and chronic phases and methods developed for in vivo neurochemical monitoring. Coupling TBI models demonstrating chronic behavioral deficits with in vivo technologies capable of real-time monitoring of neurotransmitters provides an innovative approach to directly quantify and characterize neurotransmitter signaling as a universal consequence of TBI and the direct influence of pharmacological approaches on both behavior and signaling.
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38

Mendoza, Alexander, Thomas Asrat, Favian Liu, Pauline Wonnenberg, and Alexander G. Zestos. "Carbon Nanotube Yarn Microelectrodes Promote High Temporal Measurements of Serotonin Using Fast Scan Cyclic Voltammetry." Sensors 20, no. 4 (2020): 1173. http://dx.doi.org/10.3390/s20041173.

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Carbon fiber-microelectrodes (CFMEs) have been the standard for neurotransmitter detection for over forty years. However, in recent years, there have been many advances of utilizing alternative nanomaterials for neurotransmitter detection with fast scan cyclic voltammetry (FSCV). Recently, carbon nanotube (CNT) yarns have been developed as the working electrode materials for neurotransmitter sensing capabilities with fast scan cyclic voltammetry. Carbon nanotubes are ideal for neurotransmitter detection because they have higher aspect ratios enabling monoamine adsorption and lower limits of detection, faster electron transfer kinetics, and a resistance to surface fouling. Several methods to modify CFMEs with CNTs have resulted in increases in sensitivity, but have also increased noise and led to irreproducible results. In this study, we utilize commercially available CNT-yarns to make microelectrodes as enhanced neurotransmitter sensors for neurotransmitters such as serotonin. CNT-yarn microelectrodes have significantly higher sensitivities (peak oxidative currents of the cyclic voltammograms) than CFMEs and faster electron transfer kinetics as measured by peak separation (ΔEP) values. Moreover, both serotonin and dopamine are adsorption controlled to the surface of the electrode as measured by scan rate and concentration experiments. CNT yarn microelectrodes also resisted surface fouling of serotonin onto the surface of the electrode over thirty minutes and had a wave application frequency independent response to sensitivity at the surface of the electrode.
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Shadlaghani, Arash, Mahsa Farzaneh, Dacen Kinser, and Russell C. Reid. "Direct Electrochemical Detection of Glutamate, Acetylcholine, Choline, and Adenosine Using Non-Enzymatic Electrodes." Sensors 19, no. 3 (2019): 447. http://dx.doi.org/10.3390/s19030447.

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Non-electroactive neurotransmitters such as glutamate, acetylcholine, choline, and adenosine play a critical role in proper activity of living organisms, particularly in the nervous system. While enzyme-based sensing of this type of neurotransmitter has been a research interest for years, non-enzymatic approaches are gaining more attention because of their stability and low cost. Accordingly, this focused review aims to give a summary of the state of the art of non-enzymatic electrochemical sensors used for detection of neurotransmitter that lack an electrochemically active component. In place of using enzymes, transition metal materials such as those based on nickel show an acceptable level of catalytic activity for neurotransmitter sensing. They benefit from fast electron transport properties and high surface energy and their catalytic activity can be much improved if their surface is modified with nanomaterials such as carbon nanotubes and platinum nanoparticles. However, a general comparison reveals that the performance of non-enzymatic biosensors is still lower than those that use enzyme-based methods. Nevertheless, their excellent stability demonstrates that non-enzymatic neurotransmitter sensors warrant additional research in order to advance them toward becoming an acceptable replacement for the more expensive enzyme-based sensors.
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40

Wagner, Julia, Svenja Tetzlaff, Ekin Reyhan, and Varun Venkataramani. "CNSC-56. DIVERSE, FUNCTIONAL NEUROTRANSMITTER RECEPTOR EXPRESSION ON GLIOBLASTOMA CELLS ENABLES EXTENSIVE NEURON-TO-GLIOMA COMMUNICATION." Neuro-Oncology 26, Supplement_8 (2024): viii53—viii54. http://dx.doi.org/10.1093/neuonc/noae165.0212.

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Abstract Glioblastomas are invasive yet incurable brain tumors. Recent data have shown that glutamatergic neuron-to-glioma synapses drive glioblastoma proliferation and invasion. In this study, we set out to investigate whether glioblastoma could communicate with neurons via various neuron-derived neurotransmitters through a functional neurotransmitter receptor screening. For this purpose, we stably transduced glioblastoma cells with a genetically encoded calcium indicator and sequentially and locally applied eight different neurotransmitters to glioblastoma cells in neuron-glioma co-cultures. These neurotransmitters included acetylcholine, ATP, dopamine, glutamate, GABA, adrenaline, serotonin, and glycine. We observed functional responses to acetylcholine, glutamate, ATP, dopamine, indicating a potential role for diverse neuron-to-glioma communication. Further, we investigated in patient-derived xenograft models and human tissues the existence of putative neuron-to-glioma synapses that could signal via acetlycholine, ATP and dopamine. In conclusion, this study reveals that glioblastoma cells express a heterogeneous set of functional neurotransmitter receptors, which may facilitate neuron-to-tumor communication across broad neuronal populations and warrant further investigation into their role for tumor biology.
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41

Huang, Chun-Ping, Yi-Wen Lin, Der-Yen Lee, and Ching-Liang Hsieh. "Electroacupuncture Relieves CCI-Induced Neuropathic Pain Involving Excitatory and Inhibitory Neurotransmitters." Evidence-Based Complementary and Alternative Medicine 2019 (October 20, 2019): 1–9. http://dx.doi.org/10.1155/2019/6784735.

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Neuropathic pain caused by peripheral tissue injuries to the higher brain regions still has no satisfactory therapy. Disruption of the balance of excitatory and inhibitory neurotransmitters is one of the underlying mechanisms that results in chronic neuropathic pain. Targeting neurotransmitters and related receptors may constitute a novel approach for treating neuropathic pain. We investigated the effects of electroacupuncture (EA) on chronic constriction injury- (CCI-) induced neuropathic pain. The mechanical allodynia and thermal hyperalgesia pain behaviors were relieved by 15 Hz EA but not by 2 and 50 Hz. These phenomena were associated with increasing γ-amino-butyric acid (GABA) receptors in the hippocampus and periaqueductal gray (PAG) but not N-methyl-D-aspartate receptors. Furthermore, excitatory neurotransmitter glutamate was decreased in the hippocampus and inhibitory neurotransmitter GABA was increased in the PAG under treatment with EA. These data provide novel evidence that EA modulates neurotransmitters and related receptors to reduce neuropathic pain in the higher brain regions. This suggests that EA may be a useful therapy option for treating neuropathic pain.
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42

Afanas’eva, Z. A., L. K. Mukhamatgaleeva, F. S. Bilalov, I. G. Gataullin, V. P. Potanin, and A. K. Ismagilov. "Neurotransmitter exchange in patients with skin melanoma." Kazan medical journal 98, no. 3 (2017): 323–28. http://dx.doi.org/10.17750/kmj2017-323.

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Aim. To study peculiarities of neurotransmitter exchange in patients with skin melanoma. &#x0D; Methods. Neurotransmitters (adrenaline, noradrenaline, dopamine) and their ratio in blood plasma were determined in 111 patients with skin melanoma and 38 healthy donors. The patients were divided into 3 groups: primary patients, patients with relapse of the disease and without relapse. To exclude the influence of undesirable factors (stress and physical exertion) on the level of neurotransmitters, the patients’ blood was drawn 1 day after admission in the morning on an empty stomach. Adrenaline, noradrenaline and dopamine concentration in the blood plasma was determined with the use of high-yield liquid chromatography with electrochemical detection.&#x0D; Results. Analyzing noradrenaline/adrenaline ratio in the studied patients’ groups we noted significant unidirectionality of the changes in the form of increased noradrenaline and decreased adrenergic link of sympathoadrenal system i.e. in patients with skin melanoma mediator link dominates over hormonal link. Evaluation of noradrenaline/dopamine and dopamine ratio demonstrated that in normal or even increased level of dopamine adrenaline and noradrenaline levels are below normal that can indicate dysfunction of enzyme systems involved in neurotransmitter exchange and/or their accumulation in tumors. Maximal disorders of neurotransmitter exchange were registered in the group of patients with the disease relapse. &#x0D; Conclusion. Patients with skin melanoma have imbalance of sympathoadrenal system that creates the perspective for the use of neuropharmacological drugs and psychotherapy in the treatment and rehabilitation of such patients.
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Helmschrodt, Christin, Susen Becker, Stefanie Perl, Anja Schulz, and Angelika Richter. "Development of a fast liquid chromatography-tandem mass spectrometry method for simultaneous quantification of neurotransmitters in murine microdialysate." Analytical and Bioanalytical Chemistry 412, no. 28 (2020): 7777–87. http://dx.doi.org/10.1007/s00216-020-02906-z.

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Abstract The continuous measurement of multiple neurotransmitters in microdialysate of freely moving mice to study neurochemical changes in specific brain regions requires a rapid and very sensitive quantitative analytical method. The quantitative analysis of 11 neurotransmitters and metabolites, including serotonin (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), melatonin (ME), dopamine (DA), levodopa (l-DOPA), 3-methoxytyramine (3-MT), norepinephrine (NE), epinephrine (EP), acetylcholine (ACh), choline (Ch), and γ-aminobutyric acid (GABA), was performed using a biphenyl column coupled to an API-QTrap 3200 (AB SCIEX) mass spectrometer in positive electrospray ionization mode. To the microdialysate samples, 0.5 ng of isotopically labeled standard was added for analyte quantification. A rapid liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was developed and validated for the simultaneous analysis of monoamines, their precursor, and metabolites, as well as ACh, Ch, and GABA in murine microdialysate within 7.0 min. The limit of detection in artificial CSF ranged from 0.005 ng/mL (ME) to 0.75 ng/mL (NE and GABA). A comprehensive pre-analytical protocol was validated. Recovery was between 87 and 117% for neurotransmitter concentrations from 0.6 to 45 ng/mL with an inter-day accuracy of below 20%. Basal neurotransmitter values were determined in the striatum of mice over a time period of 3 h. This LC-MS/MS method, including a short and gentle sample preparation, is suitable for simultaneous measurements of neurotransmitters in murine cerebral microdialysate and enables the determination of basal neurotransmitter levels in specific brain regions to detect disease-related and drug-induced neurochemical changes. Graphical abstract
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Tavakolian-Ardakani, Hosu, Cristea, Mazloum-Ardakani, and Marrazza. "Latest Trends in Electrochemical Sensors for Neurotransmitters: A Review." Sensors 19, no. 9 (2019): 2037. http://dx.doi.org/10.3390/s19092037.

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Neurotransmitters are endogenous chemical messengers which play an important role in many of the brain functions, abnormal levels being correlated with physical, psychotic and neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's disease. Therefore, their sensitive and robust detection is of great clinical significance. Electrochemical methods have been intensively used in the last decades for neurotransmitter detection, outclassing more complicated analytical techniques such as conventional spectrophotometry, chromatography, fluorescence, flow injection, and capillary electrophoresis. In this manuscript, the most successful and promising electrochemical enzyme-free and enzymatic sensors for neurotransmitter detection are reviewed. Focusing on the activity of worldwide researchers mainly during the last ten years (2010–2019), without pretending to be exhaustive, we present an overview of the progress made in sensing strategies during this time. Particular emphasis is placed on nanostructured-based sensors, which show a substantial improvement of the analytical performances. This review also examines the progress made in biosensors for neurotransmitter measurements in vitro, in vivo and ex vivo.
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45

Fields, R. Douglas. "Release of neurotransmitters from glia." Neuron Glia Biology 6, no. 3 (2010): 137–39. http://dx.doi.org/10.1017/s1740925x11000020.

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There is no question about the fact that astrocytes and other glial cells release neurotransmitters that activate receptors on neurons, glia and vascular cells, and that calcium is an important second messenger regulating the release. This occurs in cell culture, tissue slice and in vivo. Negative results from informative experiments designed to test the mechanism of calcium-dependent neurotransmitter release from astrocytes and the ensuing effects on synaptic transmission, have been cited as evidence calling into question whether astrocytes release neurotransmitters under normal circumstances with effects on synaptic transmission. The special feature section in this issue of Neuron Glia Biology addresses these issues and other aspects of neurotransmitter release from astrocytes in communicating with neurons and glial cells. Together these studies suggest that application of vocabulary and concepts developed for synaptic communication between neurons can lead to confusion and apparent paradoxes with respect to communication by extracellular signaling molecules released from glia in response to functional activity.
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46

King, BF. "Bombesin and Satiety." Physiology 6, no. 4 (1991): 177–80. http://dx.doi.org/10.1152/physiologyonline.1991.6.4.177.

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The abrupt cessation of feeding, before useful nutrient absorption, indicates that sensory nerves or gut hormones from the upper alimentary canal signal "preabsorptive satiety." Several neurotransmitters and hormonal substances have been identified as putative satiety agents. One candidate is bombesin, which mimics a mammalian gut-brain neurotransmitter.
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47

Mishchenko, Oksana, Natalia Palagina, Yuliia Larianovskaya, Tatyana Gorbach, Viktor Khomenko, and Nataliia Yasna. "Influence of a new derivative of 4-aminobutanoic acid on the level of neuromediatory aminoacids, neuromediators and the state of the rats’ hypocamp in conditions of brain ischemia." ScienceRise: Pharmaceutical Science, no. 2 (30) (April 30, 2021): 64–71. http://dx.doi.org/10.15587/2519-4852.2021.230305.

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The aim: to investigate the effect of a new derivative of 4-aminobutanoic acid (compounds KGM-5) on the level of neurotransmitters and neurotransmitter amino acids and the structural-functional state of the hippocampus of rats with acute cerebrovascular accident (ACVA).&#x0D; Materials and methods. ACVA was reproduced in rats by occlusion of the left carotid artery under anesthesia (sodium thiopental (35 mg/kg) intraperitoneally (i/p). 5 groups of animals were used: intact control (IC, n=6), untreated animals with ACVA (CP, n=13); animals with ACVA (n=14), which were treated for 5 days with KGM-5 at a dose of 30 mg/kg i/p, animals with ACVA (n=13), who received i/p comparison drug “Picamilon” (17 mg/kg). There was a group of pseudo-operated animals (POA, n=8). Withdrawal of animals from the experiment was performed on day 6 after modeling ACVA by painless euthanasia under anesthesia. Histological examinations of CA1 and CA3 zones of the ventral hippocampus were performed with staining of sections with thionine by the method of Nissl and hematoxylin, eosin. In the rat brain, neurotransmitter amino acids and neurotransmitters were identified. Statistical processing was performed using the W-Shapiro-Wills test to verify the normality of the distribution and the nonparametric Mann-Whitney U-test. The accepted significance level is p&lt;0.05.&#x0D; Results. Under the influence of the compound KGM-5 and “Picamilon” in the CA1 zone of the hippocampus, the number of normochromic neurons increased by 20 % and 16.6 %, respectively, hyperchromic pycnomorphic neurons and shadow cells decreased respectively by 5.8; 2.9 times and 6.3; 3.5 times, the index of alteration of neurons decreased by 6 times and 4.8 times, respectively, the area of ​​the perikaryon of these neurons increased by 39.7 % and 77.8 %, respectively, compared with KP (p&lt;0.05). Both studied agents showed a less pronounced normalizing effect on the CA3 area of the hippocampus. The new compound KGM-5 showed a normalizing effect similar to “Picamilon” on the level of neurotransmitter amino acids and neurotransmitters in the brain of rats with ACVA.&#x0D; Conclusions. Therapeutic administration of KGM-5 increases the survival of ventral hippocampal neurons, reducing the relative proportion of irreversibly altered cells, and helps to restore impaired levels of neurotransmitter amino acids and neurotransmitters in the brain of rats with ACVA.&#x0D; The neuroprotective effect of the new compound KGM-5 corresponds to this comparison drug “Picamilon”
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48

van der Mast, Rose C. "Pathophysiology of Delirium." Journal of Geriatric Psychiatry and Neurology 11, no. 3 (1998): 138–45. http://dx.doi.org/10.1177/089198879801100304.

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Hypotheses about the pathophysiology of delirium are speculative and largely based on animal research. According to the neurotransmitter hypothesis, decreased oxidative metabolism in the brain causes cerebral dysfunction due to abnormalities of various neurotransmitter systems. Reduced cholinergic function, excess release of dopamine, norepinephrine, and glutamate, and both decreased and increased serotonergic and γ-aminobutyric acid activity may underlie the different symptoms and clinical presentations of delirium. According to the inflammatory hypothesis, increased cerebral secretion of cytokines due to a wide range of physically stressful events plays an important role in the occurrence of delirium. Since cytokines can influence the activity of various neurotransmitter systems, these mechanisms may interact. Also, more fundamental processes like intraneuronal signal transduction, second messenger systems that at the same time use neurotransmitters as first messengers and play an important role in their synthesis and release, may be disturbed. Furthermore, severe illness and physiologic stress may give rise to modification of blood-brain barrier permeability, the sick euthyroid syndrome with abnormalities of thyroid hormone concentrations, and increased activity of the hypothalamic-pituitary-adrenal axis. These circumstances possibly also contribute to changes in neurotransmitter synthesis and release of cytokines in the brain, and consequently to the occurrence of delirium. Elderly patients are more at risk for developing delirium, very likely due to age-related cerebral changes in stress-regulating neurotransmitter and intracellular signal transduction systems. This paper will expand upon these current theories and discuss their applicability to research and clinical work with elderly patients suffering from delirium.
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49

Cook, Ian, Ting Wang, and Thomas S. Leyh. "Tetrahydrobiopterin regulates monoamine neurotransmitter sulfonation." Proceedings of the National Academy of Sciences 114, no. 27 (2017): E5317—E5324. http://dx.doi.org/10.1073/pnas.1704500114.

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Monoamine neurotransmitters are among the hundreds of signaling small molecules whose target interactions are switched “on” and “off” via transfer of the sulfuryl-moiety (–SO3) from PAPS (3′-phosphoadenosine 5′-phosphosulfate) to the hydroxyls and amines of their scaffolds. These transfer reactions are catalyzed by a small family of broad-specificity enzymes—the human cytosolic sulfotransferases (SULTs). The first structure of a SULT allosteric-binding site (that of SULT1A1) has recently come to light. The site is conserved among SULT1 family members and is promiscuous—it binds catechins, a naturally occurring family of flavanols. Here, the catechin-binding site of SULT1A3, which sulfonates monoamine neurotransmitters, is modeled on that of 1A1 and used to screen in silico for endogenous metabolite 1A3 allosteres. Screening predicted a single high-affinity allostere, tetrahydrobiopterin (THB), an essential cofactor in monoamine neurotransmitter biosynthesis. THB is shown to bind and inhibit SULT1A3 with high affinity, 23 (±2) nM, and to bind weakly, if at all, to the four other major SULTs found in brain and liver. The structure of the THB-bound binding site is determined and confirms that THB binds the catechin site. A structural comparison of SULT1A3 with SULT1A1 (its immediate evolutionary progenitor) reveals how SULT1A3 acquired high affinity for THB and that the majority of residue changes needed to transform 1A1 into 1A3 are clustered at the allosteric and active sites. Finally, sequence records reveal that the coevolution of these sites played an essential role in the evolution of simian neurotransmitter metabolism.
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50

Gaw, Alasdair J., Roger M. Wadsworth, and Patrick P. A. Humphrey. "Neurotransmission in the Sheep Middle Cerebral Artery: Modulation of Responses by 5-HT and Haemolysate." Journal of Cerebral Blood Flow & Metabolism 10, no. 3 (1990): 409–16. http://dx.doi.org/10.1038/jcbfm.1990.71.

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In ring sections of the sheep middle cerebral artery, electrical field stimulation elicits a complex response due to the simultaneous release of vasodilator and vasoconstrictor neurotransmitters. Haemolysate abolishes the relaxant effects of the vasodilator neurotransmitter and causes a marked augmentation of the contractile response in both the presence (448 ± 191%) and absence (409 ± 134%) of an intact endothelium. The haemolysate also reverses relaxation induced by sodium nitroprusside or sodium nitrite but has no effect on relaxation induced by 8-Br-cGMP. The vasodilator neurotransmitter therefore appears to act directly on the smooth muscle to cause relaxation by the stimulation of guanylate cyclase. The vasoconstrictor neurotransmitters that are released are antagonised by prazosin (100 n M), ketanserin (100 n M) and atropine (100 n M), which suggests that the transmitters involved are noradrenaline, 5-hydroxytryptamine (5-HT), and acetylcholine, respectively. In the presence of these three antagonists at 10 μ M, there was 86.9 ± 4.8% inhibition. Incubation with 5-HT (10 μ M) causes a marked augmentation of the contractile response (267 ± 56%) to field stimulation that can be reduced by pretreatment with either desipramine or citalopram, inhibitors of noradrenergic and serotoninergic uptake mechanisms, respectively. The 5-HT appears to be taken up into noradrenergic nerves and released as an alternative neurotransmitter upon subsequent stimulation. These actions of haemolysate and 5-HT may be involved in the cerebral vasospasm observed following subarachnoid haemorrhage.
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