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Relevant bibliographies by topics / Serotonin; Glutamate; Brain function

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Academic literature on the topic 'Serotonin; Glutamate; Brain function'

Author: Grafiati

Published: 4 June 2021

Last updated: 11 February 2022

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Journal articles on the topic "Serotonin; Glutamate; Brain function"

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Nazhmiddinovich Soliev, Nuriddin, and Odiljon Shermatovich Boymatov. "Serotonin Regulation Of Energy Metabolism Of Mitochondria Of Various Organs Of Rats." American Journal of Applied sciences 3, no. 05 (May 31, 2021): 116–22. http://dx.doi.org/10.37547/tajas/volume03issue05-18.

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Serotonin reduces the respiratory function of the mitochondria of the brain, heart and liver of rats. Serotonin significantly reduces the transport of electrons from glutamate to the oxygen molecule along the respiratory chain relative to succinate. These changes lead to a slight increase in the oxidative efficiency of phosphorylation in the oxidation of glutamate in mitochondria.

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Liu, Zhixiang, Rui Lin, and Minmin Luo. "Reward Contributions to Serotonergic Functions." Annual Review of Neuroscience 43, no. 1 (July 8, 2020): 141–62. http://dx.doi.org/10.1146/annurev-neuro-093019-112252.

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The brain serotonin systems participate in numerous aspects of reward processing, although it remains elusive how exactly serotonin signals regulate neural computation and reward-related behavior. The application of optogenetics and imaging techniques during the last decade has provided many insights. Here, we review recent progress on the organization and physiology of the dorsal raphe serotonin neurons and the relationships between their activity and behavioral functions in the context of reward processing. We also discuss several interesting theories on serotonin's function and how these theories may be reconciled by the possibility that serotonin, acting in synergy with coreleased glutamate, tracks and calculates the so-called beneficialness of the current state to guide an animal's behavior in dynamic environments.

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D’Alessandro, Giuseppina, Clotilde Lauro, Deborah Quaglio, Francesca Ghirga, Bruno Botta, Flavia Trettel, and Cristina Limatola. "Neuro-Signals from Gut Microbiota: Perspectives for Brain Glioma." Cancers 13, no. 11 (June 4, 2021): 2810. http://dx.doi.org/10.3390/cancers13112810.

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Glioblastoma (GBM) is the most aggressive form of glioma tumor in adult brain. Among the numerous factors responsible for GBM cell proliferation and invasion, neurotransmitters such as dopamine, serotonin and glutamate can play key roles. Studies performed in mice housed in germ-free (GF) conditions demonstrated the relevance of the gut-brain axis in a number of physiological and pathological conditions. The gut–brain communication is made possible by vagal/nervous and blood/lymphatic routes and pave the way for reciprocal modulation of functions. The gut microbiota produces and consumes a wide range of molecules, including neurotransmitters (dopamine, norepinephrine, serotonin, gamma-aminobutyric acid [GABA], and glutamate) that reach their cellular targets through the bloodstream. Growing evidence in animals suggests that modulation of these neurotransmitters by the microbiota impacts host neurophysiology and behavior, and affects neural cell progenitors and glial cells, along with having effects on tumor cell growth. In this review we propose a new perspective connecting neurotransmitter modulation by gut microbiota to glioma progression.

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Mathew, Sanjay J., Jeremy D. Coplan, Eric L. P. Smith, Darryle D. Schoepp, Leonard A. Rosenblum, and Jack M. Gorman. "Glutamate—Hypothalamic-Pituitary-Adrenal Axis Interactions: Implications for Mood and Anxiety Disorders." CNS Spectrums 6, no. 7 (July 2001): 555–64. http://dx.doi.org/10.1017/s1092852900002091.

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AbstractDysregulation of the hypothalamic-pituitary-adrenal (HPA) axis is a pathologic feature of certain mood and anxiety disorders that results in the increased production and secretion of corticotropin-releasing factor. There is increasing preclinical evidence that glutamate, an excitatory amino acid, plays an important role in the regulation of the HPA axis. Activation of glutamatergic projections to limbic structures such as the amygdala and brainstem structures such as the nucleus tractus solitarius is implicated in the stress response. There are laboratory and clinical suggestions that glutamatergic N-methyl-D-aspartate (NMDA) receptor antagonists function as antidepressants, and that chronic antidepressant treatments have a significant impact on NMDA receptor function. Clinical investigations of glutamate antagonists in patients with mood and anxiety disorders are in their infancy, with a few reports suggesting the presence of mood-elevating properties. Ultimately, HPA axis modulators, serotonin-enhancing agents, and glutamate antagonists might serve to increase neurotropic factors in key brain regions for affective and anxiety regulation, providing a putative final common pathway.

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Kim, Jong-Hoon, János Marton, Simon Mensah Ametamey, and Paul Cumming. "A Review of Molecular Imaging of Glutamate Receptors." Molecules 25, no. 20 (October 16, 2020): 4749. http://dx.doi.org/10.3390/molecules25204749.

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Molecular imaging with positron emission tomography (PET) and single photon emission computed tomography (SPECT) is a well-established and important in vivo technique to evaluate fundamental biological processes and unravel the role of neurotransmitter receptors in various neuropsychiatric disorders. Specific ligands are available for PET/SPECT studies of dopamine, serotonin, and opiate receptors, but corresponding development of radiotracers for receptors of glutamate, the main excitatory neurotransmitter in mammalian brain, has lagged behind. This state of affairs has persisted despite the central importance of glutamate neurotransmission in brain physiology and in disorders such as stroke, epilepsy, schizophrenia, and neurodegenerative diseases. Recent years have seen extensive efforts to develop useful ligands for molecular imaging of subtypes of the ionotropic (N-methyl-D-aspartate (NMDA), kainate, and AMPA/quisqualate receptors) and metabotropic glutamate receptors (types I, II, and III mGluRs). We now review the state of development of radioligands for glutamate receptor imaging, placing main emphasis on the suitability of available ligands for reliable in vivo applications. We give a brief account of the radiosynthetic approach for selected molecules. In general, with the exception of ligands for the GluN2B subunit of NMDA receptors, there has been little success in developing radiotracers for imaging ionotropic glutamate receptors; failure of ligands for the PCP/MK801 binding site in vivo doubtless relates their dependence on the open, unblocked state of the ion channel. Many AMPA and kainite receptor ligands with good binding properties in vitro have failed to give measurable specific binding in the living brain. This may reflect the challenge of developing brain-penetrating ligands for amino acid receptors, compounded by conformational differences in vivo. The situation is better with respect to mGluR imaging, particularly for the mGluR5 subtype. Several successful PET ligands serve for investigations of mGluRs in conditions such as schizophrenia, depression, substance abuse and aging. Considering the centrality and diversity of glutamatergic signaling in brain function, we have relatively few selective and sensitive tools for molecular imaging of ionotropic and metabotropic glutamate receptors. Further radiopharmaceutical research targeting specific subtypes and subunits of the glutamate receptors may yet open up new investigational vistas with broad applications in basic and clinical research.

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Sander, Christin Y., Hanne D. Hansen, and Hsiao-Ying Wey. "Advances in simultaneous PET/MR for imaging neuroreceptor function." Journal of Cerebral Blood Flow & Metabolism 40, no. 6 (March 13, 2020): 1148–66. http://dx.doi.org/10.1177/0271678x20910038.

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Hybrid imaging using PET/MRI has emerged as a platform for elucidating novel neurobiology, molecular and functional changes in disease, and responses to physiological or pharmacological interventions. For the central nervous system, PET/MRI has provided insights into biochemical processes, linking selective molecular targets and distributed brain function. This review highlights several examples that leverage the strengths of simultaneous PET/MRI, which includes measuring the perturbation of multi-modal imaging signals on dynamic timescales during pharmacological challenges, physiological interventions or behavioral tasks. We discuss important considerations for the experimental design of dynamic PET/MRI studies and data analysis approaches for comparing and quantifying simultaneous PET/MRI data. The primary focus of this review is on functional PET/MRI studies of neurotransmitter and receptor systems, with an emphasis on the dopamine, opioid, serotonin and glutamate systems as molecular neuromodulators. In this context, we provide an overview of studies that employ interventions to alter the activity of neuroreceptors or the release of neurotransmitters. Overall, we emphasize how the synergistic use of simultaneous PET/MRI with appropriate study design and interventions has the potential to expand our knowledge about the molecular and functional dynamics of the living human brain. Finally, we give an outlook on the future opportunities for simultaneous PET/MRI.

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Baj, Andreina, Elisabetta Moro, Michela Bistoletti, Viviana Orlandi, Francesca Crema, and Cristina Giaroni. "Glutamatergic Signaling Along The Microbiota-Gut-Brain Axis." International Journal of Molecular Sciences 20, no. 6 (March 25, 2019): 1482. http://dx.doi.org/10.3390/ijms20061482.

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A complex bidirectional communication system exists between the gastrointestinal tract and the brain. Initially termed the “gut-brain axis” it is now renamed the “microbiota-gut-brain axis” considering the pivotal role of gut microbiota in maintaining local and systemic homeostasis. Different cellular and molecular pathways act along this axis and strong attention is paid to neuroactive molecules (neurotransmitters, i.e., noradrenaline, dopamine, serotonin, gamma aminobutyric acid and glutamate and metabolites, i.e., tryptophan metabolites), sustaining a possible interkingdom communication system between eukaryota and prokaryota. This review provides a description of the most up-to-date evidence on glutamate as a neurotransmitter/neuromodulator in this bidirectional communication axis. Modulation of glutamatergic receptor activity along the microbiota-gut-brain axis may influence gut (i.e., taste, visceral sensitivity and motility) and brain functions (stress response, mood and behavior) and alterations of glutamatergic transmission may participate to the pathogenesis of local and brain disorders. In this latter context, we will focus on two major gut disorders, such as irritable bowel syndrome and inflammatory bowel disease, both characterized by psychiatric co-morbidity. Research in this area opens the possibility to target glutamatergic neurotransmission, either pharmacologically or by the use of probiotics producing neuroactive molecules, as a therapeutic approach for the treatment of gastrointestinal and related psychiatric disorders.

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SOYTURK, Hayriye, Bihter Gökçe BOZAT, Hamit COŞKUN, and Fatma PEHLİVAN KARAKAŞ. "The effect of intra-amygdalar leptin administration on anxiety, depression and learning behaviors in rats." Journal of Experimental and Clinical Medicine 38, no. 3 (April 23, 2021): 331–35. http://dx.doi.org/10.52142/omujecm.38.3.24.

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Leptin is released by adipose tissue. Leptin can cross the blood–brain barrier and bind to receptors on neurons in brain areas to exert its biological function when released into circulation. This study aimed to determine the influences of intra-amygdalar administration of high and low doses of leptin on anxiety, depression, learning behaviors of rats. In the experimental protocol I, intra-amygdalar injection of high and low doses of leptin (0.1 and 1 μg/ kg) and saline were administered 30 min before the behavioral tests. Then, the animals were exposed to open field, elevated plus maze, Porsolt and Morris water maze tests for measuring of behaviors. In experimental protocol 2, the cerebrospinal fluids of all groups of experimental protocol 1 were collected by microdialysis method and then were analyzed by HPLC. The effect of the low dose of leptin was significant on the open field. The effect of the high and low dose of leptin was significant on the elevated plus maze test. The effect of the low dose of leptin was significant on mobility in the center of the Porsolt. A high dose of leptin group had spent less time around the platform than controls in the Morris water maze test. HPLC analysis showed that the amount of serotonin and glutamate in the amygdala region increased after low dose leptin administration. Intra-amygdalar injection of low doses of leptin may decrease anxiety and depression-like behavior in rats by increasing serotonin and glutamate levels in the amygdala.

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Takagi, Yasushi, Masaki Nishimura, Asuka Morizane, Jun Takahashi, Kazuhiko Nozaki, Junya Hayashi, and Nobuo Hashimoto. "Survival and differentiation of neural progenitor cells derived from embryonic stem cells and transplanted into ischemic brain." Journal of Neurosurgery 103, no. 2 (August 2005): 304–10. http://dx.doi.org/10.3171/jns.2005.103.2.0304.

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Object. Cell replacement therapy including the use of embryonic stem cells (ESCs) may represent a novel treatment for damage from stroke. In this study, the authors transplanted neural progenitor cells (NPCs) derived from ESCs into ischemic brain and analyzed their survival and differentiation. Methods. Multipotential NPCs were generated from ESCs by using the stromal cell—derived inducing activity method. These cells could differentiate in vitro into neurons, glia, and oligodendrocytes, thus revealing them to be neural stem cells. The NPCs were then transplanted into ischemic brain. At 2 weeks postischemia, the transplanted cells occupied 18.8 ± 2.5% of the hemispheric area; by 4 weeks postischemia, 26.5 ± 4% of the hemisphere. At 4 weeks after transplantation, green fluorescent protein (GFP)—positive transplanted cells showed mature neuronal morphological features. The authors also investigated the expression of differentiation markers and various neurotransmitters. Transplanted cells were immunopositive for neuronal nuclei, β-tubulin-III, and glial fibrillary acidic protein. Of the GFP-positive cells, 33.3 ± 11.5% were positive for glutamate decarboxylase, 13.3 ± 5.8% for glutamate, 2.1 ± 2.5% for tyrosine hydroxylase, 1.8 ± 2% for serotonin, and 0.4 ± 0.2% for choline acetyltransferase. Conclusions. The authors confirmed the survival and differentiation of ESC-derived NPCs transplanted into the ischemic brain. Surviving transplanted cells expressed several neural markers and neurotransmitters. These findings indicate that these cells can function in the brain.

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Stȩpień, A., M. Chalimoniuk, and J. Strosznajder. "Serotonin 5HT1B/1D Receptor Agonists Abolish NMDA Receptor-evoked Enhancement of Nitric Oxide Synthase Activity and cGMP Concentration in Brain Cortex Slices." Cephalalgia 19, no. 10 (December 1999): 859–65. http://dx.doi.org/10.1046/j.1468-2982.1999.1910859.x.

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Our previous studies indicating that the function of excitatory amino acids, NMDA type receptor, is modulated by serotonin focused on the interaction between serotonin 5HT1B/1D and glutamate, NMDA receptor in brain cortex. The effect of agonists of 5HT1B/1D receptor, sumatriptan, and zolmitriptan on NMDA receptor-evoked activation of nitric oxide (NO) and cGMP synthesis in adult rat brain cortex slices was investigated. Two kinds of experiment were carried out using adult rats. In one of them, sumatriptan or zolmitriptan was administered in vivo subcutaneously (s.c.) in a dose of 0.1 mg per kg body weight. Brain slices were then prepared and used in the experiments or, in the other exclusively in vitro studies, both agonists at 10 μM concentration were added directly to the incubation medium containing adult rat brain cortex slices. The data obtained from these studies indicated that stimulation of NMDA receptor in brain cortex slices. The data obtained from these studies indicated that stimulation of NMDA receptor in brain cortex slices leads to a large increase in calcium, calmodulin-dependent NO synthase (NOS) activity and to significant enhancement of the cGMP level. This NMDA receptor-dependent NO and cGMP release was completely blocked by competitive and noncompetitive NMDA receptor antagonists APV (10 μM) or MK-801 (10 μM.), respectively. The specific inhibitor of Ca2+-dependent isoforms of NOS (N-nitro-1-arginine NNLA and 7-nitroindozole (7-N1)) eliminated the NMDA receptor-mediated enhancement of NO and cGMP release. Moreover, the serotonin 5HT1B/1D receptor agonists sumatriptan and zolmitriptan administrated in vivo (s.c.) or in vitro abolished NMDA receptor-evoked NO signalling in brain cortex. The potency of both agonists investigated directly in vitro was similar to their effect after in vivo administration. These results suggest that both serotonin 5HT1B/1D receptor agonists may play an important role in modulating the NO and cGMP-dependent signal transduction pathway in the brain. This effect of sumatriptan and zolmitriptan on NO signaling in the brain system should be taken into consideration when investigating their mechanism of action in the migraine attack.

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Dissertations / Theses on the topic "Serotonin; Glutamate; Brain function"

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Mellor, Robert. "Neurochemical studies on cultured glial cells." Thesis, University of Oxford, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300038.

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Taylor, Matthew John. "The effect of serotonin reuptake inhibition on brain glutamate." Thesis, University of Oxford, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510244.

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Maron, Eduard. "Serotonin function in panic disorder: from clinical experiments to brain imaging and genetics /." Online version, 2004. http://dspace.utlib.ee/dspace/bitstream/10062/557/5/maron.pdf.

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Sundaram, Hardy. "Characterisation of recombinant human serotonin 5-HTâ†1â†A receptors expressed in Chinese hamster ovary cells." Thesis, University of Kent, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.262508.

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Furmark, Tomas. "Social Phobia. From Epidemiology to Brain Function." Doctoral thesis, Uppsala University, Department of Psychology, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-546.

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Social phobia is a disabling anxiety disorder characterized by an excessive fear of negative evaluation in social situations. The present thesis explored the epidemiology and neurobiology of the disorder. By means of a mailed questionnaire, the point prevalence of social phobia in the Swedish general population was estimated at 15.6%. However, prevalence rates varied between 1.9 and 20.4% across the different levels of distress and impairment used to define cases. Thus, although social anxiety is widespread within the community, the precise diagnostic boundaries for social phobia are difficult to determine. Social phobia was associated with female gender, low educational attainment, psychoactive medication use, and lack of social support. A cluster analysis revealed that subtypes of social phobia mainly differed dimensionally on a mild-moderate-severe continuum, with number of cases declining with increasing severity. Public speaking was the most common social fear in all groups of social phobics and in the population at large.

In the neurobiological studies, positron emission tomography was used to examine brain serotonin metabolism and changes in the regional cerebral blood flow (rCBF) response to public speaking stress following treatment with a selective serotonin reuptake inhibitor (SSRI) or cognitive-behavioral group therapy. Social phobics exhibited lowered serotonin turnover, relative to non-phobics, mainly in the medial temporal cortex including the bilateral rhinal and periamygdaloid regions. Symptom improvement with cognitive-behavioral- as well as SSRI-treatment was accompanied by a reduced rCBF-response to public speaking in the amygdala, hippocampus and adjacent temporal cortex, i.e. regions that serve important functions in anxiety. Thorough suppression of rCBF in limbic brain regions was associated with favorable long-term treatment outcome. These results provide neuroimaging evidence for a presynaptic serotonergic dysfunction in social phobia and for a common neural mechanism whereby psychological and pharmacological anti-anxiety treatments act.

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Dwyer, Daniel, and na. "Serotonin as a Mediator of Fatigue During Exercise and Training." Griffith University. School of Health Science, 2004. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20040521.130535.

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Exercise has been shown to cause an increase in the concentration of brain serotonin (5-hydroxytryptamine, 5-HT) in humans and experimental animals. The increase in brain serotonin coincides with the onset of fatigue and is referred to as "central fatigue". Experiments in humans and animals involving serotonin receptor agonists have demonstrated reductions in exercise performance by simulating the exercise-induced increase in endogenous serotonin. Conversely, the administration of serotonin receptor antagonists has been shown to extend exercise performance in experimental animals, but not in humans. Although the relationship between the concentration of brain serotonin and exercise performance is well described in the literature, the precise effect of central fatigue on muscle function per se is unclear. Furthermore, there appear to be differences in serotonergic function between trained and untrained cohorts. However, it is not clear whether the differences are due to a training adaptation or if the differences are inherent in the individual. In addition, the time course of these adaptations and the mechanisms of adaptation are not known. The initial purpose of this thesis was to determine whether six weeks of endurance exercise training had any effect on central serotonin receptor sensitivity in Wistar rats. The rats ran on a treadmill 4 times per week with 2 exercise tests of endurance performance per week. Receptor sensitivity was determined indirectly, at the end of each training week, by the reduction in endurance performance, under the influence of a 5-HT1a agonist, (m-Chlorophenylpiperazine, m-CPP). Improved tolerance to the fatiguing effects of the serotonin agonist would suggest desensitisation of central serotonin receptors, probably 5-HT1a receptors. Two groups of controls were used to examine, i) the effect of the injection per se on exercise performance and ii) changes in serotonin receptor sensitivity associated with maturation, in the absence of any exercise training. In the training group, undrugged exercise performance significantly improved by 47% after 6 weeks of training (mean ± SEM, 4518 ± 729 s vs. 6640 ± 903 s, p=0.01). Drugged exercise performance also increased significantly from week 1 to week 6 (306 ± 69 s to 712 ± 192 s, p=0.004). Control group results indicated that the dose of m-CPP alone caused fatigue during exercise tests and that maturation was not responsible for any decrease in receptor sensitivity. Endurance training appears to stimulate an adaptive response to the fatiguing effects of increased brain serotonin, which may enhance endurance exercise performance. The purpose of the second set of experiments described in this thesis was to investigate changes in serotonin receptor sensitivity in response to exercise training in human subjects. Twelve male volunteers completed 30 minutes of stationary cycling at 70% of VO2peak, on 3 days per week, for 9 weeks. Serotonin receptor sensitivity was assessed indirectly by measuring the prolactin response to a serotonin receptor agonist (buspirone hydrochloride), using a placebo controlled, blind cross-over design. A sedentary group of control subjects were also recruited to control for possible seasonal variations in serotonin receptor sensitivity. Endurance capacity was also assessed as time to exhaustion while cycling at 60% of VO2peak. The exercise training caused a significant increase in aerobic power (VO2peak, 3.1±0.16 to 3.6±0.15 L.m-1, p< 0.05) and endurance capacity (93±8 to 168±11 min, p<0.05), but there was no change (p>0.05) in the prolactin response to a serotonin agonist. However, 25% of the subjects in the training group demonstrated a decrease in receptor sensitivity, as indicated by a decrease in prolactin response. These results suggest that while the exercise training caused an increase in aerobic power and endurance capacity, there was no measurable change in 5-HT receptor sensitivity. In addition, it is possible that changes in receptor sensitivity may take longer to occur, the training stimulus used in the present investigation was inadequate or that changes occurred in other 5-HT receptor subtypes that were not assessed by the present methodology. The third set of experiments described here, investigated the changes in neuromuscular function under the influence of a serotonin receptor agonist (buspirone hydrochloride). Subjects were administered the agonist or a placebo in a blind cross over design. Measures of neuromuscular function included reaction time (RT), hand eye coordination (HEC), isometric neuromuscular control (INC), maximal voluntary isometric contractile force (MVIC-F), isometric muscular endurance capacity (IMEC) and various electromyographic (EMG) indices of fatigue in biceps brachii. A preliminary experiment was conducted to determine a drug dose that did not cause sedation of the research subjects. The agonist caused a significant (p<0.05) decrease in MVIC-F, INC and IMEC. There was a non significant (p = 0.08) decrease in EMG amplitude during the MVIC-F trial with the agonist, compared to the effect of the placebo. The median EMG frequency during the IMEC test was also significantly less with the agonist, when compared to the placebo effect. There was a decline in RT and HEC, although this was not significant. These findings indicate that a serotonin receptor agonist causes a decrease in neuromuscular function during isometric muscle contractions. The decrements in muscle function reported in this study may help to explain previous reports of an association between increased brain serotonin concentration and a reduction in endurance performance. Although the present study does not exclude the possibility that an increase in brain serotonin does cause fatigue by affecting organs peripheral to the brain, it provides evidence of fatigue within the central nervous system. Further examination of the effect of a serotonin agonist on muscle function during non-isometric muscle contractions is warranted.

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Elhusseiny, Ahmed. "Functional acetylcholine and serotonin receptors in brain microcirculation : importance of subtype and cellular localization in the determination of function." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0032/NQ64553.pdf.

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Rylands, Angela J. "An investigation of cognitive function and the brain serotonin (5HT) system in impulsive aggression (IA), using positron emission tomography." Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511920.

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Wang, Dongsha. "The state of DNA methylation of serotonin transporter (SLC6A4) in peripheral T cells and monocytes is associated with aggression and central 5-HT function; DNA methylation as biomarkers of brain function." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=107671.

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Aggressive behaviour is a complex phenomenon that often arises in early childhood and typically decreases with age. Studies have shown that adults with severe aggression often have lower serotonin (5-HT) neurotransmission. The hypothesis of this thesis is that 5-HT alterations associated with childhood aggression are also defined by epigenetic mechanisms through differential methylation of critical genes in the 5-HT pathway that can be detected in peripheral white blood cells. Serotonin transporter (SLC6A4) was chosen in this study based on its importance in 5-HT function and preliminary genomic DNA microarray data. We first determined the state of DNA methylation of SLC6A4 promoter using pyrosequencing in T cells and monocytes isolated from blood of adult males with low or high childhood-limited aggression (N=25) and who have been followed since childhood. We then examined whether the state of DNA methylation of SLC6A4 promoter in the blood is associated with in vivo measures of brain 5-HT synthesis by integrating previously obtained Positron emission tomography (PET) data from these participants. Lastly, a luciferase reporter construct was generated to test whether SLC6A4 promoter methylation plays a functional role in its transcriptional activity. Significantly higher levels of methylation in high childhood-limited physical aggression (C-LHPA) group were observed in both T cells and monocytes at specific CpG sites. In addition, greater mean methylation of significantly altered CpGs was associated with lower 5-HT synthesis in the left and right lateral orbitofrontal cortex (OBFC) in both cells (N = 20). Moreover, in vitro methylation of the SLC6A4 promoter dramatically suppressed gene expression suggesting that methylation plays a functional role in gene regulation. Taken all together, these novel findings imply that SLC6A4 is epigenetically modulated by DNA methylation and that DNA methylation is associated with in aggression level observed during childhood. The association between higher DNA methylation and lower brain 5-HT synthesis supports the relevance of using DNA methylation in peripheral white blood cells as a marker for human brain 5-HT function. If these results can be confirmed in a larger sample, the identification of such 5-HT biomarkers may be beneficial for the prediction, prevention and evaluation of treatment of psychiatric disorders with 5-HT involvement.
Le comportement agressif est un phénomène complexe qui survient souvent lors de la petite enfance et diminue typiquement avec l'âge. Des études ont montré qu'une agressivité sévère chez l'adulte est associée à une plus faible neurotransmission de sérotonine (5-HT). L'hypothèse de cette thèse est que les modifications de neurotransmission de 5-HT associées à l'agressivité infantile sont également dépendantes de mécanismes epigénétiques, notamment du niveau de méthylation des gènes critiques à la régulation de la neurotransmission de la 5-HT qui peut être mesuré dans les leucocytes périphériques. Le transporteur de la sérotonine (SLC6A4) a été choisi dans cette étude dû à son importance dans la régulation du niveau de 5-HT ainsi qu'au vu de données provenant d'analyses préliminaires de micropuces d'ADN génomique. Nous avons premièrement déterminé les niveaux de méthylation d'ADN du promoteur de SLC6A4 en utilisant la méthode de pyroséquençage dans des cellules T et des monocytes isolés à partir de sang prélevé chez des hommes adultes ayant présenté des niveaux d'agressivité faibles ou importants durant l'enfance (N=25). Nous avons ensuite examiné si les niveaux de méthylation d'ADN du promoteur de SLC6A4 mesurés dans les cellules sanguines sont corrélés aux niveaux de synthèse cérébrale de 5-HT mesurés in vivo par tomographie par émission de positrons (TEP) chez les mêmes participants. Enfin, nous avons évalué in vitro grâce à une technique utilisant le gène rapporteur luciférase si le niveau de méthylation du promoteur de SLC6A4 est directement impliqué dans la modulation de son niveau de transcription. Nous avons mesuré des niveaux de méthylation de CpG spécifiques de SLC6A4 significativement plus importants dans les cellules T ainsi que dans les monocytes du groupe d'hommes ayant présentés une forte agressivité durant l'enfance (C-LHPA) par rapport au groupe ayant présenté une faible agressivité durant l'enfance. De plus, nous avons montré que ces niveaux de méthylation importants sont associés à une synthèse réduite de 5-HT au sein des cortex orbitofrontaux latéraux (OBFC) gauche et droit (N = 20). De plus, nous avons mesuré in vitro que la méthylation du promoteur SLC6A4 réprime fortement son expression. Ces données suggèrent que le niveau d'expression de SLC6A4 est modulé épigénétiquement par la méthylation de l'ADN et que les niveaux de méthylation du gène corrèlent avec les niveaux d'agressivité observés durant l'enfance. L'association entre les niveaux de méthylation d'ADN et de synthèse cérébral de 5-HT renforce la pertinence d'utiliser les niveaux de méthylation d'ADN de leucocytes périphériques comme indicateur du niveau de neurotransmission de 5-HT cérébrale. Ces résultats demandent à être confirmés au sein d'une cohorte plus importante. Cependant, l'identification d'un tel marqueur biologique pourrait être utile à la prédiction, la prévention et l'évaluation de traitements de désordres psychiatriques associés à des problèmes de neurotransmission de 5-HT.

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Yin, Weiling. "Brain control of reproductive aging : GnRH neuroterminal, glia and portal capillary interactions." Thesis, 2008. http://hdl.handle.net/2152/29693.

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Reproductive function is essential to the survival of all species. In mammals and other vertebrates, the control of reproduction relies on the hypothalamic-pituitary-gonadal axis, with the primary driving force provided by hypothalamic GnRH neurons. In the median eminence, the decapeptide GnRH are released in a unique pattern from GnRH neuroterminals into the portal capillary system as part of reproductive cycle. During aging, the biological rhythms of GnRH release are altered in a species-specific manner, with a reduction of GnRH pulsatility and surge in aging female rats resulting in reproductive senescence, which happens much earlier than gonadal failure in rats. Relatively few studies have focused on regulation of GnRH release at the neuroterminal level in the median eminence during reproductive aging. Therefore, the aims of this dissertation are to 1) Study the regulation of GnRH secretion at the neuroterminal level, focusing on glutamate transmission; 2) Ascertain the interaction between GnRH neuroterminals and their surrounding microenvironment focused on glial cells and the portal capillary system in the median eminence; and 3) Analyze age and hormone effects on GnRH neuroterminals and their microenvironment. An aging ovariectomized female rat model was used to study the effects of age and hormones on GnRH neuroterminal system. Fluorescence microscopy, confocal microscopy and transmission electron microscopy were used in conjunction with several imaging analysis tools. I mastered the use of cryo-embedding multi-probe immunogold labeling electron microscopy, which was essential to visualize and quantify the ultrastructral changes in GnRH neuroterminals. I combined the serial electron microscopy with cryo-embedding immunogold electron microscopy preparation and developed a new technique to examine biological markers with a three-dimensional perspective at the cellular level. Results from a series of four research projects showed: 1) There is a novel glutermatergic pathway in GnRH neuroterminals, which may regulate GnRH secretion; 2) There are dramatic age related morphological changes in the GnRH neuroterminal /glia/ portal capillary system of the median eminence that may be involved in reproductive senescence and other neuroendocrine system impairments with age; 3) Serial electron microscopy combined with immunogold labeling technique is a useful method to study the regulation of neuronal signaling pathway. Although my studies were performed on a rat model, it seems reasonable to predict that some of these changes in the median eminence with age may apply to other species, including humans, relevant to some of the menopausal symptoms in women.
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Books on the topic "Serotonin; Glutamate; Brain function"

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Serotonin, '91 Conference (1991 Birmingham England). Serotonin, CNS receptors, and brain function: Proceedings of the Serotonin '91 Conference held in Birmingham, United Kingdom, on 14-17 July 1991. Oxford: Pergamon, 1992.

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International Meeting on Metabotropic Glutamate Receptors (2nd 1996 Taormina, Italy). Metabotropic glutamate receptors and brain function: Proceedings of the 2nd International Meeting on Metabotropic Glutamate Receptors held in Taormina, Italy, in September 1996. Edited by Moroni F, Nicoletti F, and Pellegrini-Giampietro D. E. London: Portland, 1998.

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Friedel, Robert O., and Stephen M. Stahl. The Fundamentals of Brain Neurotransmission. Edited by Christian Schmahl, K. Luan Phan, Robert O. Friedel, and Larry J. Siever. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199362318.003.0002.

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This chapter outlines the fundamental principles underlying neuroscience, particularly as it relates to neurotransmission and neuropharmacology. It then reviews and synthesizes of the role of different neurochemical and neurotransmitter systems that underlie brain function and synaptic transmission, including GABA, glutamate, serotonin, dopamine, norepinephrine, acetylcholine, and histamine. In addition, it describes various psychoactive medications are used in the treatment of personality disorders, such as mood stabilizers and antipsychotics. Moreover, it describes how these agents target these systems by describing their different mechanisms of action. It provides a primer to better understand the pathophysiology and pharmacological treatment of personality disorders discussed in the book.

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Fanning, Jennifer R., and Emil F. Coccaro. Neurobiology of Impulsive Aggression. Edited by Phillip M. Kleespies. Oxford University Press, 2015. http://dx.doi.org/10.1093/oxfordhb/9780199352722.013.24.

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Aggression is a behavior with evolutionary origins, but in today’s society it’s often both destructive and maladaptive. The fact that aggression has a strong basis in biological factors has long been apparent from case histories of traumatic brain damage. Research over the past several decades has confirmed the involvement of neurotransmitter function and abnormalities in brain structure and function in aggressive behavior. This research has centered around the “serotonin hypothesis” and on dysfunction in prefrontal brain regions. As this literature continues to grow, guided by preclinical research and aided by the application of increasingly sophisticated neuroimaging methodology, a more complex picture has emerged, implicating diverse neurotransmitter and neuropeptide systems (e.g., glutamate, vasopressin, and oxytocin) and neural circuits. As the current pharmacological and therapeutic interventions are effective but imperfect, it is hoped that new insights into the neurobiology of aggression will reveal novel avenues for treatment of this destructive and costly behavior.

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Robbins, Trevor. The Neuropsycho–Pharmacology of Attention. Edited by Anna C. (Kia) Nobre and Sabine Kastner. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199675111.013.028.

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Pharmacological influences on cognition and behaviour are often accompanied by effects on different aspects of attention. The actions of many psychoactive drugs (often used in the treatment of psychiatric disorders) depend on effects exerted on the classical chemical modulatory neurotransmitter systems including acetylcholine, and the monoamines, dopamine, noradrenaline and serotonin (or 5-hydroxytryptamine, 5-HT). These chemical systems originate in the reticular core of the brain and modulate attention by actions on forebrain structures including the thalamus, striatum, and the neocortex (especially the prefrontal cortex). Current research is attempting to dissect separable functions of these chemical neurotransmitters in mediating attention in relation to states of arousal and stress in comparable test paradigms in experimental animals and humans. New directions in research in this area are also identified, including the functions of the novel neurotransmitter orexin, and the role of GABA and glutamate in gamma oscillations and the network properties of the neocortex.

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Bradley, P. B. Serotonin, CNS Receptors and Brain Function. Pergamon, 1993.

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Bradley, P. B. Serotonin, CNS Receptors and Brain Function. Pergamon, 1993.

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(Editor), F. Moroni, D. E. Pellegrini-Giampietro (Editor), and F. Nicoletti (Editor), eds. Metabotropic Glutamate Receptors and Brain Function (Portland Press Proceedings,). Ashgate Publishing, 1998.

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Elizabeth Cornelia H. De Rooy. Effects of depressing brain serotonin function on adrenergically-induced feeding in rats. 1987.

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Serotonin 1991: 5-Hydroxytryptamine - CNS receptors and brain function : international conference held under the auspices of the Serotonin Club, 14th-17th July, Birmingham University, Birmingham UK. [s.n.]: [s.l.], 1991.

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Book chapters on the topic "Serotonin; Glutamate; Brain function"

1

Shen, Jun. "NMR Spectroscopy of Brain Glutamate Function." In Neuromethods, 83–115. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7228-9_4.

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Murphy, Dennis L., Joseph Zohar, Brian A. Lawlor, Trey Sunderland, Teresa A. Pigott, Charanjit S. Aulakh, Gyorgy Bagdy, and Nancy A. Garrick. "Hormonal Responses to Serotonergic Drugs as a Means to Evaluate Brain Serotonergic Function in Humans." In Serotonin, 565–80. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-009-1912-9_74.

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Fernstrom, John D. "Tryptophan Availability and Serotonin Synthesis in Brain." In Amino Acid Availability and Brain Function in Health and Disease, 137–46. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73175-4_12.

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Sakimura, Kenji. "Molecular Structure and Physiological Function of the Glutamate Receptor Channel." In Molecular Biology and Brain Ischemia, 13–27. Tokyo: Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-68467-1_2.

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Leathwood, P. "Dietary Manipulation of Serotonin and Behaviour." In Amino Acid Availability and Brain Function in Health and Disease, 275–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73175-4_25.

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Michaelis, E. K., J. W. Chen, T. M. Stormann, and S. Roy. "Molecular and Functional Characterization of a Brain Neuronal Membrane Glutamate-Binding Protein." In Neurotransmitters and Cortical Function, 71–83. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0925-3_5.

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Cowen, P. J. "Neuroendocrine Responses to Tryptophan as an Index of Brain Serotonin Function." In Amino Acid Availability and Brain Function in Health and Disease, 285–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73175-4_26.

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Praschak-Rieder, Nicole, and Matthaeus Willeit. "Imaging of Seasonal Affective Disorder and Seasonality Effects on Serotonin and Dopamine Function in the Human Brain." In Brain Imaging in Behavioral Neuroscience, 149–67. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/7854_2011_174.

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Lookingland, K. J., N. J. Shannon, and K. E. Moore. "Effects of Tryptophan Administration on the Synthesis, Storage and Metabolism of Serotonin in the Hypothalamus of Normal and Raphe-Stimulated Rats." In Amino Acid Availability and Brain Function in Health and Disease, 159–66. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73175-4_14.

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Anderson, I., and P. Cowen. "Neuroendocrine Responses to L-Tryptophan as an Index of Brain Serotonin Function: Effect of Weight Loss." In Advances in Experimental Medicine and Biology, 245–54. Boston, MA: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4684-5952-4_22.

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