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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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Syvälahti, E. K. G. "Biological Factors in Schizophrenia Structural and Functional Aspects." British Journal of Psychiatry 164, S23 (April 1994): 9–14. http://dx.doi.org/10.1192/s0007125000292672.
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A number of factors have been proposed as being linked to schizophrenia: genetic, psychological, endocrinological, metabolic, environmental, virological, and auto-immunological factors, as well as neurotransmitter systems and structural disorders of the brain. All may act as predisposing, triggering, or functionally modulating factors in what is probably a condition composed of several types of disorder with varying aetiology. Neuroanatomical and neuromorphological data have revealed ventricular enlargement and diminished frontal and temporal lobe volume in some patients. These changes are concentrated particularly in the hippocampus/parahippocampal gyrus/amygdala, but are relatively small and span some overlap with healthy subjects. Twin studies suggest that at least some of these changes may result from other than genetic factors. Functional disturbances of the brain have also been connected with frontal and temporal structures in some schizophrenic patients. Of the single neurotransmitter substances, dopamine and serotonin appear to represent some of the central restitutive mechanisms whose function is to maintain mental stability; the understanding of their interplay with other neurotransmitters such as noradrenaline, acetylcholine, GABA, and glutamate, should provide a more integrated view of both normal and disturbed brain function.
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Andreas, Plaitakis. "Modulation of Monoaminergic and Amino Acid Transmission as a Means for Therapeutic Intervention in Ataxia." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 20, S3 (May 1993): S105—S108. http://dx.doi.org/10.1017/s0317167100048605.
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ABSTRACT:In recent years, substantial progress has been made in understanding the organization and function of the cerebellum at the neuronal, synaptic, and molecular level. More than any other region of the brain, the cerebellum utilizes amino acids as its main excitatory and inhibitory transmitters. Excitatory amino acids, such as glutamate and aspartate, in addition to serving as chemical messengers, may also mediate neurodegenerative processes in human ataxic disorders. Of the monoamines, serotonin has been proposed as a neuromodulator in the cerebellum and is thought to play a role in the pathophysiology of ataxia in animal models, and human cerebellar disorders. These considerations raise the possibility that pharmacologic modification of amino acid and serotonergic transmission may provide a means for therapeutic intervention in ataxia.
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Shen, Yanbin, and Sung Woo Kim. "45 Opportunity with functional role of supplemental amino acids." Journal of Animal Science 97, Supplement_2 (July 2019): 24. http://dx.doi.org/10.1093/jas/skz122.045.
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Abstract The technological advancement in production of crystalline amino acids has driven the cost of crystalline amino acids down significantly and facilitated the wide use of crystalline amino acids in food animal production. The primary reason of use of crystalline amino acids in am animal’s diet is to provide dietary essential nutrients for protein synthesis and to balance the diet and reduce dietary cost. Extensive researches with amino acids have greatly enabled such use. As a result, most swine diets today are formulated with 3 or 4 supplemental amino acids. However, the economical return on including beyond 4 supplemental amino acids becomes low and thus discourages the use of more than 4 supplemental amino acids for dietary saving purpose. The use of the functional role of amino acids might bear the new opportunity for amino acids. Tryptophan has unique physiological functions involving synthesize serotonin in the body. Increasing tryptophan intake is shown to elevate serotonin synthesis in the brain of pigs and reduce stress and improve performance of pigs under social stress. Research shows that methionine is used as a precursor of glutathione to protect intestinal mucosa from oxidative damages during weaning stress. Arginine, glutamine, and glutamate are shown to have functions in cell proliferation, potentially improving intestinal and immune function of nursery pigs and preventing loss of lean body mass in the sow. Leucine is a ketogenic amino acid. The carbon skeleton of leucine is converted to acetylCoA, which could be used for fatty acid synthesis in muscle tissue. Research showed that intramuscular fat was increased by feeding high dietary leucine levels. Overall, the different functions of individual AA beyond their roles as the building blocks for proteins give additional opportunities of amino acid application in animal production.
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Phillips, Joseph R., Abeer M. Eissa, Doaa H. Hewedi, Marjan Jahanshahi, Mohamed El-Gamal, Szabolcs Keri, and Ahmed A. Moustafa. "Neural substrates and potential treatments for levodopa-induced dyskinesias in Parkinson’s disease." Reviews in the Neurosciences 27, no. 7 (October 1, 2016): 729–38. http://dx.doi.org/10.1515/revneuro-2016-0009.
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AbstractParkinson’s disease (PD) is primarily a motor disorder that involves the gradual loss of motor function. Symptoms are observed initially in the extremities, such as hands and arms, while advanced stages of the disease can effect blinking, swallowing, speaking, and breathing. PD is a neurodegenerative disease, with dopaminergic neuronal loss occurring in the substantia nigra pars compacta, thus disrupting basal ganglia functions. This leads to downstream effects on other neurotransmitter systems such as glutamate, γ-aminobutyric acid, and serotonin. To date, one of the main treatments for PD is levodopa. While it is generally very effective, prolonged treatments lead to levodopa-induced dyskinesia (LID). LID encompasses a family of symptoms ranging from uncontrolled repetitive movements to sustained muscle contractions. In many cases, the symptoms of LID can cause more grief than PD itself. The purpose of this review is to discuss the possible clinical features, cognitive correlates, neural substrates, as well as potential psychopharmacological and surgical (including nondopaminergic and deep brain stimulation) treatments of LID.
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Herian, Monika, Mateusz Skawski, Adam Wojtas, Małgorzata K. Sobocińska, Karolina Noworyta, and Krystyna Gołembiowska. "Tolerance to neurochemical and behavioral effects of the hallucinogen 25I-NBOMe." Psychopharmacology 238, no. 8 (May 25, 2021): 2349–64. http://dx.doi.org/10.1007/s00213-021-05860-5.
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Abstract Rationale 4-Iodo-2,5-dimethoxy-N-(2-methoxybenzyl)phenethylamine (25I-NBOMe) is a potent serotonin 5-HT2A/2C receptor agonist with hallucinogenic activity. There is no data on the 25I-NBOMe effect on brain neurotransmission and animal performance after chronic administration. Objectives We examined the effect of a 7-day treatment with 25I-NBOMe (0.3 mg/kg/day) on neurotransmitters’ release and rats’ behavior in comparison to acute dose. Methods Changes in dopamine (DA), serotonin (5-HT), acetylcholine (ACh), and glutamate release were studied using microdialysis in freely moving rats. The hallucinogenic activity was measured in the wet dog shake (WDS) test. The animal locomotion was examined in the open field (OF) test, short-term memory in the novel object recognition (NOR) test. The anxiogenic/anxiolytic properties of the drug were tested using the light/dark box (LDB) test. Results Repeated administration of 25I-NBOMe decreased the response to a challenge dose of DA, 5-HT, and glutamatergic neurons in the frontal cortex as well as weakened the hallucinogenic activity in comparison to acute dose. In contrast, striatal and accumbal DA and 5-HT release and accumbal but not striatal glutamate release in response to the challenge dose of 25I-NBOMe was increased in comparison to acute treatment. The ACh release was increased in all brain regions. Behavioral tests showed a motor activity reduction and memory deficiency in comparison to a single dose and induction of anxiety after the drug’s chronic and acute administration. Conclusions Our findings suggest that multiple injections of 25I-NBOMe induce tolerance to hallucinogenic activity and produce alterations in neurotransmission. 25I-NBOMe effect on short-term memory, locomotor function, and anxiety seems to be the result of complex interactions between neurotransmitter pathways.
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Pehrson, Alan L., Theepica Jeyarajah, and Connie Sanchez. "Regional distribution of serotonergic receptors: a systems neuroscience perspective on the downstream effects of the multimodal-acting antidepressant vortioxetine on excitatory and inhibitory neurotransmission." CNS Spectrums 21, no. 2 (August 7, 2015): 162–83. http://dx.doi.org/10.1017/s1092852915000486.
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Previous work from this laboratory hypothesized that the multimodal antidepressant vortioxetine enhances cognitive function through a complex mechanism, using serotonergic (5-hydroxytryptamine, 5-HT) receptor actions to modulate gamma-butyric acid (GABA) and glutamate neurotransmission in key brain regions like the prefrontal cortex (PFC) and hippocampus. However, serotonergic receptors have circumscribed expression patterns, and therefore vortioxetine’s effects on GABA and glutamate neurotransmission will probably be regionally selective. In this article, we attempt to develop a conceptual framework in which the effects of 5-HT, selective serotonin reuptake inhibitors (SSRIs), and vortioxetine on GABA and glutamate neurotransmission can be understood in the PFC and striatum—2 regions with roles in cognition and substantially different 5-HT receptor expression patterns. Thus, we review the anatomy of the neuronal microcircuitry in the PFC and striatum, anatomical data on 5-HT receptor expression within these microcircuits, and electrophysiological evidence on the effects of 5-HT on the behavior of each cell type. This analysis suggests that 5-HT and SSRIs will have markedly different effects within the PFC, where they will induce mixed effects on GABA and glutamate neurotransmission, compared to the striatum, where they will enhance GABAergic interneuron activity and drive down the activity of medium spiny neurons. Vortioxetine is expected to reduce GABAergic interneuron activity in the PFC and concomitantly increase cortical pyramidal neuron firing. However in the striatum, vortioxetine is expected to increase activity at GABAergic interneurons and have mixed excitatory and inhibitory effects in medium spiny neurons. Thus the conceptual framework developed here suggests that vortioxetine will have regionally selective effects on GABA and glutamate neurotransmission.
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Ballaz, Santiago. "The unappreciated roles of the cholecystokinin receptor CCK(1) in brain functioning." Reviews in the Neurosciences 28, no. 6 (July 26, 2017): 573–85. http://dx.doi.org/10.1515/revneuro-2016-0088.
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AbstractThe CCK(1) receptor is a G-protein-coupled receptor activated by the sulfated forms of cholecystokinin (CCK), a gastrin-like peptide released in the gastrointestinal tract and mammal brain. A substantial body of research supports the hypothesis that CCK(1)r stimulates gallbladder contraction and pancreatic secretion in the gut, as well as satiety in brain. However, this receptor may also fulfill relevant roles in behavior, thanks to its widespread distribution in the brain. The strategic location of CCK(1)r in mesolimbic structures and specific hypothalamic and brainstem nuclei lead to complex interactions with neurotransmitters like dopamine, serotonin, and glutamate, as well as hypothalamic hormones and neuropeptides. The activity of CCK(1)r maintains adequate levels of dopamine and regulates the activity of serotonin neurons of raphe nuclei, which makes CCK(1)r an interesting therapeutic target for the development of adjuvant treatments for schizophrenia, drug addiction, and mood disorders. Unexplored functions of CCK(1)r, like the transmission of interoceptive sensitivity in addition to the regulation of hypothalamic hormones and neurotransmitters affecting emotional states, well-being, and attachment behaviors, may open exciting roads of research. The absence of specific ligands for the CCK(1) receptor has complicated the study of its distribution in brain so that research about its impact on behavior has been published sporadically over the last 30 years. The present review reunites all this body of evidence in a comprehensive way to summarize our knowledge about the actual role of CCK in the neurobiology of mental illness.
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Bulgakova, S., and N. Romanchuk. "The Participation of Hormones in the Processes of Cognitive and Socio-Emotional Aging." Bulletin of Science and Practice 6, no. 8 (August 15, 2020): 97–129. http://dx.doi.org/10.33619/2414-2948/57/09.
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Aging is associated with generally accepted changes in brain functions, including cognitive ones. In addition, age makes its own adjustments to the work of the endocrine system. In turn, a change in the hormonal background during the aging process imprints the work of brain cells, cognitive functions, and socio-emotional functioning. Investigated, the relationship between sex hormones, cortisol, oxytocin and cognitive and socio-emotional functioning. Sex hormones are involved in neurite growth, synaptogenesis, dendritic branching, myelination, and other important mechanisms of neural plasticity. Physiological and pathological conceptualized theories suggest how sex hormones potentially cause neuroplasticity changes through four neurochemical neurotransmitter systems: serotonin, dopamine, GABA and glutamate. Many brain regions express high density estrogen and progesterone receptors such as the amygdala, hypothalamus, and hippocampus. The hippocampus is of particular importance in the context of mediating structural plasticity in the adult brain, differences in behavior, neurochemical patterns and structure of the hippocampus with a changing hormonal environment have been investigated. There is a significant association between emotion dysregulation and symptoms of depression, anxiety, eating pathology, and substance abuse. Higher levels of emotion regulation are associated with a high level of social competence.
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Sardar, Debosmita, Brittney Lozzi, Junsung Woo, Teng-Wei Huang, Caroline Cvetkovic, Chad J. Creighton, Robert Krencik, and Benjamin Deneen. "Mapping Astrocyte Transcriptional Signatures in Response to Neuroactive Compounds." International Journal of Molecular Sciences 22, no. 8 (April 12, 2021): 3975. http://dx.doi.org/10.3390/ijms22083975.
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Astrocytes play central roles in normal brain function and are critical components of synaptic networks that oversee behavioral outputs. Despite their close affiliation with neurons, how neuronal-derived signals influence astrocyte function at the gene expression level remains poorly characterized, largely due to difficulties associated with dissecting neuron- versus astrocyte-specific effects. Here, we use an in vitro system of stem cell-derived astrocytes to identify gene expression profiles in astrocytes that are influenced by neurons and regulate astrocyte development. Furthermore, we show that neurotransmitters and neuromodulators induce distinct transcriptomic and chromatin accessibility changes in astrocytes that are unique to each of these neuroactive compounds. These findings are highlighted by the observation that noradrenaline has a more profound effect on transcriptional profiles of astrocytes compared to glutamate, gamma-aminobutyric acid (GABA), acetylcholine, and serotonin. This is demonstrated through enhanced noradrenaline-induced transcriptomic and chromatin accessibility changes in vitro and through enhanced calcium signaling in vivo. Taken together, our study reveals distinct transcriptomic and chromatin architecture signatures in astrocytes in response to neuronal-derived neuroactive compounds. Since astrocyte function is affected in all neurological disorders, this study provides a new entry point for exploring genetic mechanisms of astrocyte–neuron communication that may be dysregulated in disease.
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Lennertz, Leonhard, Petra E. Franke, Hans Jörgen Grabe, Friederike Rampacher, Svenja Schulze-Rauschenbach, Vera Guttenthaler, Stephan Ruhrmann, et al. "The functional coding variant Asn107Ile of the neuropeptide S receptor gene (NPSR1) influences age at onset of obsessive–compulsive disorder." International Journal of Neuropsychopharmacology 16, no. 9 (October 1, 2013): 1951–58. http://dx.doi.org/10.1017/s1461145713000382.
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Abstract Neuropeptide S (NPS) is a novel central acting neuropeptide that modulates several brain functions. NPS has shown strong anxiolytic-like effects and interactions with other central transmitter systems, including serotonin and glutamate. A coding variation (Asn107Ile) of the NPS receptor gene (NPSR1) was associated with panic disorder and schizophrenia. Based on these encouraging findings, the present study aimed at exploring a potential role of NPSR1 in obsessive–compulsive disorder (OCD). A sample of 232 OCD patients was successfully genotyped for the NPSR1 Asn107Ile variant (rs324981). Age at onset was taken into account to address the heterogeneity of the OCD phenotype. The NPSR1 genotype significantly affected age at onset of the OCD patients, with a mean age at onset approximately 4 yr earlier in homozygous carriers of the low-functioning Asn107 variant compared to patients with at least one Ile107 variant (p = 0.032). Case–control analyses with 308 healthy control subjects reveal a highly significant association of the Asn107 variant with early onset OCD (odds ratio = 2.36, p = 0.0004) while late onset OCD or the OCD group as a whole were unrelated to the NPSR1 genotype. Based on our association finding relating NPSR1 genotype to early onset OCD, we suggest a differential role of the NPS system in OCD. In particular, the early onset OCD subtype seems to be characterized by a genetically driven low NPS tone, which might affect other OCD-related transmitter systems, including the serotonin and glutamate systems. In agreement with preclinical research, we suggest that NPS may be a promising pharmacological candidate with anti-obsessional properties.
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Ostrowski, Tim D., Daniela Ostrowski, Eileen M. Hasser, and David D. Kline. "Depressed GABA and glutamate synaptic signaling by 5-HT1A receptors in the nucleus tractus solitarii and their role in cardiorespiratory function." Journal of Neurophysiology 111, no. 12 (June 15, 2014): 2493–504. http://dx.doi.org/10.1152/jn.00764.2013.
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Serotonin (5-HT), and its 5-HT1A receptor (5-HT1AR) subtype, is a powerful modulator of the cardiorespiratory system and its sensory reflexes. The nucleus tractus solitarii (nTS) serves as the first central station for visceral afferent integration and is critical for cardiorespiratory reflex responses. However, the physiological and synaptic role of 5-HT1ARs in the nTS is relatively unknown. In the present study, we examined the distribution and modulation of 5-HT1ARs on cardiorespiratory and synaptic parameters in the nTS. 5-HT1ARs were widely distributed to cell bodies within the nTS but not synaptic terminals. In anesthetized rats, activation of 5-HT1ARs by microinjection of the 5-HT1AR agonist 8-OH-DPAT into the caudal nTS decreased minute phrenic neural activity via a reduction in phrenic amplitude. In brain stem slices, 8-OH-DPAT decreased the amplitude of glutamatergic tractus solitarii-evoked excitatory postsynaptic currents, and reduced overall spontaneous excitatory nTS network activity. These effects persisted in the presence of GABAA receptor blockade and were antagonized by coapplication of 5-HT1AR blocker WAY-100135. 5-HT1AR blockade alone had no effect on tractus solitarii-evoked excitatory postsynaptic currents, but increased excitatory network activity. On the other hand, GABAergic nTS-evoked inhibitory postsynaptic currents did not change by activation of the 5-HT1ARs, but spontaneous inhibitory nTS network activity decreased. Blocking 5-HT1ARs tended to increase nTS-evoked inhibitory postsynaptic currents and inhibitory network activity. Taken together, 5-HT1ARs in the caudal nTS decrease breathing, likely via attenuation of afferent transmission, as well as overall nTS network activity.
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Carvalhão Gil, L., M. Lázaro, A. Ponte, J. Teixeira, H. Prata Ribeiro, and T. Mota. "Treatment of alcoholism – New targets?" European Psychiatry 41, S1 (April 2017): s859. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1713.
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IntroductionAlcohol use disorders (AUD) is a preventable cause of significant morbidity and mortality worldwide. AUD is a heterogeneous disorder stemming from a complex interaction of neurobiological, genetic, and environmental factors. To achieve treatment effectiveness this heterogenity should be considered, as well as safety.ObjectivesReview mechanisms underlying alcohol addiction in order to work out new, more effective treatment strategies.AimTo update on treatment for alcoholism.MethodsA literature search was performed on PubMed database.ResultsAlcohol dependence is a chronic, relapsing condition in which there is evidence of significant change in the motivation and control systems in the brain. Increasingly drug therapy is focused not just on the treatment of the acute withdrawal syndrome, but on modifying these other dysregulated brain systems. Of the numerous neurotransmitter systems that have been identified for the development of new medicines, the most promising compounds appear to be those that modulate the function of opioids, glutamate with or without gamma-aminobutyric acid, and serotonin. Other putative therapeutic medications including direct modulators of dopamine function and enzyme inhibitors also shall be discussed. At present, only four medications are approved for the treatment of alcohol dependence in Europe, that is naltrexone, acamprosate, disulfiram and the most recent nalmefene. Among other promising strategies the following drugs are mentioned: baclofen, topiramate, ondansetron, aripiprazole, rimonabant and varenicline.ConclusionsPharmacological development remains a high priority in the alcoholism field. Drugs have different safety profiles that need to be balanced with the treatment objective, individual patient preferences and comorbid conditions.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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Praptomojati, Ardian. "“How Do I Stop Checking Things?” Understanding Obsessive-Compulsive Disorder from Neuropsychological Perspective." Buletin Psikologi 27, no. 1 (June 14, 2019): 15. http://dx.doi.org/10.22146/buletinpsikologi.32807.
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Obsessive-compulsive disorder (OCD) is the fourth most common mental disorder and WHO classifies it as one of the ten most disabling medical conditions. OCD patients have difficulty in controlling the disturbing thoughts accompanied by ritualistic behavior performed by the patient as a way to reduce anxiety or fear that leads to distress and significant dysfunction in their everyday life. Studies using neuroimaging techniques indicated a number of abnormal functions in the orbitofrontal cortex and caudate nuclei in OCD patients. Abnormalities in one or more neurotransmitters such as serotonin, glutamate, GABA, and dopamine were also found to be associated with the mechanism of the brain circuitry associated with OCD symptoms. Genetic factors were proven to also contribute considerably to OCD. This article is a literature study on OCD, especially from a neuropsychological perspective highlighting the recent development of various techniques and methods of study.
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Olatunji, Sunday, Philip Ogunnaike, Joshua Owolabi, Ayodeji Abijo, Adeshina Alabi, Stephen Adelodun, John Olanrewaju, and Adeola Adelabi. "Investigating the Effects of Allium sativum on the Prefrontal Cortex in Lithium Chloride Pilocarpine-Induced Epilepsy in Wistar Rat." NIgerian Journal of Neuroscience 12, no. 2 (August 31, 2021): 56–66. http://dx.doi.org/10.47081/njn2021.12.2/003.
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The prefrontal cortex (PFC), mediating executive brain functions is impaired in epilepsy. Allium sativum (AS) anti-seizure potential on the PFC of experimentally-induced epilepsy was investigated. Forty-eight male Wistar rats (200-250g) were randomized into six groups. Control (2mL/kg distilled water); AS only (100mg/kg); LiCl+PC (lithium chloride, 127mg/kg, and pilocarpine, 30mg/kg); LiCl+PC+AS100mg/kg and LiCl+PC+AS300mg/kg received LiCl+PC and 100mg/kg AS and 300mg/kg AS respectively; LiCl+PC+SV received LiCl+PC and sodium valproate (10mg/kg). Treatments lasted for 21 days, behavioural tests then preceded sacrifice. Brain tissues were excised, fixed in 10% neutral buffered formalin for demonstration of PFC cytoarchitecture and glial fibrillary acidic protein (GFAP) expression. Neurotransmitters were also assayed. Walling and rearing frequencies reduced significantly (p<0.05) in the LiCl+PC group compared to control. Glutamate and acetylcholine levels increased in all groups except AS only, while gamma-aminobutyric acid, dopamine, serotonin and norepinephrine levels increased in the LiCl+PC+AS100mg/kg, LiCl+PC+AS300mg/kg and LiCl+PC+SV groups compared to the control. Cytochrome C oxidase and glucose-6-phosphate dehydrogenase activities significantly increased (p<0.05) in all groups, while nitric oxide levels increased in the LiCl+PC+AS300mg/kg and LiCl+PC+SV groups compared to the control. Cytoarchitecturally, the LiCl+PC PFC showed neurodegenerative features, increased GFAP expression, while the treated groups showed preserved neurons and mild astrogliosis. Conclusively, AS showed neuroprotective potentials against LiCl+PC-induced neuronal degeneration, mitigated reactive PFC astrogliosis. However, AS did not lower glutamate and other neurotransmitter levels.
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Jessy, J., A. M. Mans, M. R. DeJoseph, and R. A. Hawkins. "Hyperammonaemia causes many of the changes found after portacaval shunting." Biochemical Journal 272, no. 2 (December 1, 1990): 311–17. http://dx.doi.org/10.1042/bj2720311.
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1. Portacaval shunting in rats results in several metabolic alterations similar to those seen in patients with hepatic encephalopathy. The characteristic changes include: (a) diminution of cerebral function; (b) raised plasma ammonia and brain glutamine levels; (c) increased neutral amino acid transport across the blood-brain barrier; (d) altered brain and plasma amino acid levels; and (e) changes in brain neurotransmitter content. The aetiology of these abnormalities remains unknown. 2. To study the degree to which ammonia could be responsible, rats were made hyperammonaemic by administering 40 units of urease/kg body weight every 12 h and killing the rats 48 h after the first injection. 3. The changes observed in the urease-treated rats were: (a) whole-brain glucose use was significantly depressed, whereas the levels of high-energy phosphates remained unchanged; (b) the permeability of the blood-brain to barrier to two large neutral amino acids, tryptophan and leucine, was increased; (c) blood-brain barrier integrity was maintained, as indicated by the unchanged permeability-to-surface-area product for acetate; (d) plasma and brain amino acid concentrations were altered; and (e) dopamine, 5-hydroxytryptamine (serotonin) and noradrenaline levels in brain were unchanged, but 5-hydroxyindoleacetic acid (5-HIAA), a metabolite of 5-hydroxytryptamine, was elevated. 4. The depressed brain glucose use, increased tryptophan permeability-to-surface-area product, elevated brain tryptophan content and rise in the level of cerebral 5-HIAA were closely correlated with the observed rise in brain glutamine content. 5. These results suggest that many of the metabolic alterations seen in rats with portacaval shunts could be due to elevated ammonia levels. Furthermore, the synthesis or accumulation of glutamine may be closely linked to cerebral dysfunction in hyperammonaemia.
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Kvarta, Mark D., Keighly E. Bradbrook, Hannah M. Dantrassy, Aileen M. Bailey, and Scott M. Thompson. "Corticosterone mediates the synaptic and behavioral effects of chronic stress at rat hippocampal temporoammonic synapses." Journal of Neurophysiology 114, no. 3 (September 2015): 1713–24. http://dx.doi.org/10.1152/jn.00359.2015.
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Chronic stress is thought to impart risk for depression via alterations in brain structure and function, but contributions of specific mediators in generating these changes remain unclear. We test the hypothesis that stress-induced increases in corticosterone (CORT), the primary rodent glucocorticoid, are the key mediator of stress-induced depressive-like behavioral changes and synaptic dysfunction in the rat hippocampus. In rats, we correlated changes in cognitive and affective behavioral tasks (spatial memory consolidation, anhedonia, and neohypophagia) with impaired excitatory strength at temporoammonic-CA1 (TA-CA1) synapses, an archetypical stress-sensitive excitatory synapse. We tested whether elevated CORT was sufficient and necessary to generate a depressive-like behavioral phenotype and decreased excitatory signaling observed at TA-CA1 after chronic unpredictable stress (CUS). Chronic CORT administration induced an anhedonia-like behavioral state and neohypophagic behavior. Like CUS, chronic, but not acute, CORT generated an impaired synaptic phenotype characterized by reduced α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-preferring glutamate receptor-mediated excitation at TA-CA1 synapses, decreased AMPA-type glutamate receptor subunit 1 protein expression, and altered serotonin-1B receptor-mediated potentiation. Repeatedly blunting stress-induced increases of CORT during CUS with the CORT synthesis inhibitor metyrapone (MET) prevented these stress-induced neurobehavioral changes. MET also prevented the CUS-induced impairment of spatial memory consolidation. We conclude that corticosterone is sufficient and necessary to mediate glutamatergic dysfunction underlying stress-induced synaptic and behavioral phenotypes. Our results indicate that chronic excessive glucocorticoids cause specific synaptic deficits in the hippocampus, a major center for cognitive and emotional processing, that accompany stress-induced behavioral dysfunction. Maintaining excitatory strength at stress-sensitive synapses at key loci throughout corticomesolimbic reward circuitry appears critical for maintaining normal cognitive and emotional behavior.
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Moroz, Leonid L., Daria Y. Romanova, and Andrea B. Kohn. "Neural versus alternative integrative systems: molecular insights into origins of neurotransmitters." Philosophical Transactions of the Royal Society B: Biological Sciences 376, no. 1821 (February 8, 2021): 20190762. http://dx.doi.org/10.1098/rstb.2019.0762.
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Transmitter signalling is the universal chemical language of any nervous system, but little is known about its early evolution. Here, we summarize data about the distribution and functions of neurotransmitter systems in basal metazoans as well as outline hypotheses of their origins. We explore the scenario that neurons arose from genetically different populations of secretory cells capable of volume chemical transmission and integration of behaviours without canonical synapses. The closest representation of this primordial organization is currently found in Placozoa, disk-like animals with the simplest known cell composition but complex behaviours. We propose that injury-related signalling was the evolutionary predecessor for integrative functions of early transmitters such as nitric oxide, ATP, protons, glutamate and small peptides. By contrast, acetylcholine, dopamine, noradrenaline, octopamine, serotonin and histamine were recruited as canonical neurotransmitters relatively later in animal evolution, only in bilaterians. Ligand-gated ion channels often preceded the establishment of novel neurotransmitter systems. Moreover, lineage-specific diversification of neurotransmitter receptors occurred in parallel within Cnidaria and several bilaterian lineages, including acoels. In summary, ancestral diversification of secretory signal molecules provides unique chemical microenvironments for behaviour-driven innovations that pave the way to complex brain functions and elementary cognition.This article is part of the theme issue ‘Basal cognition: multicellularity, neurons and the cognitive lens'.
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Tziakouri, Andria, Eszter Lajkó, and Laszlo Kohidai. "The Phylogenetic Background of Neurotransmitters in the Unicellular Organism Tetrahymena Pyriformis." Annals of Behavioral Neuroscience 1, no. 1 (October 29, 2018): 108–18. http://dx.doi.org/10.18314/abne.v1i1.1229.
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The Human Central Nervous System (CNS) is governed by electrochemical networks forming a delicate interplay between the different regions of the brain. The objective of the present experiment is to investigate the phylogenetic background of this electrochemical network by creating a comparable binary and ternary interplay of interactions between different neurotransmitters (noradrenaline, histamine, serotonin, acetylcholine, glutamate, and dopamine) in the unicellular eukaryote Tetrahymena pyriformis. Tetrahymena – as a protozoon – has no nervous system; however, it has been shown that it has not only the ability to store, synthesize and secrete biogenic amines but it also bears binding sites for the corresponding receptors of some of these molecules. The chemotactic responsiveness elicited by the neurotransmitters was examined in Tetrahymena cells, using a modified version of Leick’s two-chamber capillary chemotaxis assay with 20-minute incubation times. The concentration course of each neurotransmitter was determined and the concentration eliciting the strongest effect was further used to examine the chemotactic response of the neurotransmitters when used in pairs and in groups of three. Adequate cellular responses (chemoattractant and chemorepellent) were detected in both cases when the neurotransmitters were used alone and in combinations. A pattern detected in these responses was related to the neurotransmitters’ physicochemical characteristics (XlogP, TPSA). These provide evidence that the chief regulatory molecules of the CNS can be identified even in lower, eukaryotic unicellular levels of phylogeny and possibly alter the basic functions of these organisms. In summary, our results support the theory that any evolved nervous system-like interplay could stem from a common origin. Therefore, identifying the “ancient” function of a molecule or its receptor effect can open new windows in the advancement of therapeutic interventions.
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Chaves, Tiago, Csilla Lea Fazekas, Krisztina Horváth, Pedro Correia, Adrienn Szabó, Bibiána Török, Krisztina Bánrévi, and Dóra Zelena. "Stress Adaptation and the Brainstem with Focus on Corticotropin-Releasing Hormone." International Journal of Molecular Sciences 22, no. 16 (August 23, 2021): 9090. http://dx.doi.org/10.3390/ijms22169090.
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Stress adaptation is of utmost importance for the maintenance of homeostasis and, therefore, of life itself. The prevalence of stress-related disorders is increasing, emphasizing the importance of exploratory research on stress adaptation. Two major regulatory pathways exist: the hypothalamic–pituitary–adrenocortical axis and the sympathetic adrenomedullary axis. They act in unison, ensured by the enormous bidirectional connection between their centers, the paraventricular nucleus of the hypothalamus (PVN), and the brainstem monoaminergic cell groups, respectively. PVN and especially their corticotropin-releasing hormone (CRH) producing neurons are considered to be the centrum of stress regulation. However, the brainstem seems to be equally important. Therefore, we aimed to summarize the present knowledge on the role of classical neurotransmitters of the brainstem (GABA, glutamate as well as serotonin, noradrenaline, adrenaline, and dopamine) in stress adaptation. Neuropeptides, including CRH, might be co-localized in the brainstem nuclei. Here we focused on CRH as its role in stress regulation is well-known and widely accepted and other CRH neurons scattered along the brain may also complement the function of the PVN. Although CRH-positive cells are present on some parts of the brainstem, sometimes even in comparable amounts as in the PVN, not much is known about their contribution to stress adaptation. Based on the role of the Barrington’s nucleus in micturition and the inferior olivary complex in the regulation of fine motoric—as the main CRH-containing brainstem areas—we might assume that these areas regulate stress-induced urination and locomotion, respectively. Further studies are necessary for the field.
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Menani, Jose V., Laurival A. De Luca, and Alan Kim Johnson. "Role of the lateral parabrachial nucleus in the control of sodium appetite." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 306, no. 4 (February 15, 2014): R201—R210. http://dx.doi.org/10.1152/ajpregu.00251.2012.
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In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review.
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Mosienko, Valentina, Daniel Beis, Massimo Pasqualetti, Jonas Waider, Susann Matthes, Fatimunnisa Qadri, Michael Bader, and Natalia Alenina. "Life without brain serotonin: Reevaluation of serotonin function with mice deficient in brain serotonin synthesis." Behavioural Brain Research 277 (January 2015): 78–88. http://dx.doi.org/10.1016/j.bbr.2014.06.005.
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Saito, Hideya. "Overview: Serotonin receptors and brain function." Japanese Journal of Pharmacology 67 (1995): 53. http://dx.doi.org/10.1016/s0021-5198(19)46181-7.
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Nakanishi, S. "Roles of glutamate receptors in brain function." Biological Psychiatry 42, no. 1 (July 1997): 164S. http://dx.doi.org/10.1016/s0006-3223(97)87556-7.
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Praschak-Rieder, N., M. Willeit, H. Sitte, J. H. Meyer, and S. Kasper. "FC29-05 - Season, sunlight, and brain serotonin function." European Psychiatry 26, S2 (March 2011): 1981. http://dx.doi.org/10.1016/s0924-9338(11)73684-7.
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IntroductionMany experience low mood and energy during winter. Brain serotonin is involved in the regulation of many physiologic and pathologic functions that vary with season. Seasonal variations in peripheral serotonergic markers have been described in clinical and nonclinical populations, and a postmortem study shows seasonal differences in hypothalamic serotonin concentration.AimWe investigated the molecular background of seasonal changes in serotonin function by conducting a series of studies on serotonin transporter (5-HTT) density and function in depression and health.MethodsIn a large study in drug-free patients with seasonal affective disorder (SAD) we aimed at detecting state-related alterations in 5-HTT-mediated inward and outward transport in platelets. Another study in healthy subjects aimed at detecting seasonal variations in 5-HTT binding in the living human brain using [11C] DASB positron emission tomography. Regional 5-HTT binding, an index of 5-HTT density, was assessed in a large sample of drug-naïve healthy volunteers, and was related to meteorological and astronomical data.ResultsIn patients with SAD we showed that the 5-HTT is in a hyperfunctional state during winter depression, and normalizes after light therapy and in natural summer remission. In healthy subjects, 5-HTT binding was higher in autumn/winter as compared to spring/summer. Regional 5-HTT binding correlated negatively with daily sunshine, such that higher values occurred at times of lesser light.ConclusionsSince high 5-HTT density is associated with low synaptic serotonin levels, regulation of 5-HTT density and 5-HTT function by light is a mechanism that may explain seasonal changes in normal and pathologic behaviours.
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Jacobs, B. L., and E. C. Azmitia. "Structure and function of the brain serotonin system." Physiological Reviews 72, no. 1 (January 1, 1992): 165–229. http://dx.doi.org/10.1152/physrev.1992.72.1.165.
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Schoepp, Darryle D., and P. Jeffrey Conn. "Metabotropic glutamate receptors in brain function and pathology." Trends in Pharmacological Sciences 14, no. 1 (January 1993): 13–20. http://dx.doi.org/10.1016/0165-6147(93)90107-u.
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Kokoshka, Jerry M., Ryan R. Metzger, Diana G. Wilkins, James W. Gibb, Glen R. Hanson, and Annette E. Fleckenstein. "Methamphetamine treatment rapidly inhibits serotonin, but not glutamate, transporters in rat brain." Brain Research 799, no. 1 (July 1998): 78–83. http://dx.doi.org/10.1016/s0006-8993(98)00472-7.
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García-García, Alvaro L., Elisabet Venzala, Natalia Elizalde, M. J. Ramírez, Ahinoa Urbiola, Joaquin Del Rio, Laurence Lanfumey, and Rosa M. Tordera. "Regulation of serotonin (5-HT) function by a VGLUT1 dependent glutamate pathway." Neuropharmacology 70 (July 2013): 190–99. http://dx.doi.org/10.1016/j.neuropharm.2012.11.005.
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Labban, Ranyah Shaker M., Hanan Alfawaz, Ahmed T. Almnaizel, Wail M. Hassan, Ramesa Shafi Bhat, Nadine MS Moubayed, Geir Bjørklund, and Afaf El-Ansary. "High-fat diet-induced obesity and impairment of brain neurotransmitter pool." Translational Neuroscience 11, no. 1 (June 1, 2020): 147–60. http://dx.doi.org/10.1515/tnsci-2020-0099.
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AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.
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Fadda, F. "Tryptophan-Free Diets: A Physiological Tool to Study Brain Serotonin Function." Physiology 15, no. 5 (October 2000): 260–64. http://dx.doi.org/10.1152/physiologyonline.2000.15.5.260.
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Tryptophan-free diets produce a specific reduction of brain serotonin synthesis and release. This method for lowering neural serotonin function has been extensively used in both laboratory animals and humans to study the role of serotonin in a variety of behaviors, such as aggressiveness, sleep, sexual behavior, anxiety, mood, memory, and so forth.
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van Heeringen, C. "Suicide, Serotonin, and the Brain." Crisis 22, no. 2 (March 2001): 66–70. http://dx.doi.org/10.1027//0227-5910.22.2.66.
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Summary: The involvement of impaired serotonergic functioning in the development of suicidal behavior is one of the best documented findings in biological psychiatry. It is, however, less clear in which way this dysfunction contributes to the occurrence of suicidal behavior. Correlational studies have demonstrated associations between peripheral measures of serotonergic function and characteristics such as impulsivity, disinhibition, anxiety, and/or behavioral inhibition. Postmortem and neuroimaging studies have provided insight in the localization of serotonergic dysfunction in the central nervous system. Nevertheless, results in this area of research have also been contradictory. Following a short overview of recent research findings on serotonin and suicidal behavior, this paper focuses on the involvement of the prefrontal cortex of the brain in the development of suicidal behavior and on the role of serotonin in its executive functions. Based on these considerations, suggestions for future research are discussed.
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Carhart-Harris, RL, and DJ Nutt. "Serotonin and brain function: a tale of two receptors." Journal of Psychopharmacology 31, no. 9 (August 31, 2017): 1091–120. http://dx.doi.org/10.1177/0269881117725915.
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Haney, Megan M., Joseph Sinnott, Kate L. Osman, Ian Deninger, Ellyn Andel, Victoria Caywood, Alexis Mok, et al. "Mice Lacking Brain-Derived Serotonin Have Altered Swallowing Function." Otolaryngology–Head and Neck Surgery 161, no. 3 (April 30, 2019): 468–71. http://dx.doi.org/10.1177/0194599819846109.
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The intricate sensorimotor neural circuits that control swallowing are heavily reliant on serotonin (5-hydroxytryptamine [5-HT]); however, the impact of 5-HT deficiency on swallow function remains largely unexplored. We investigated this using mice deficient in tryptophan-hydroxylase-2 (TPH2), the enzyme catalyzing the rate-limiting step in 5-HT synthesis. Videofluoroscopy was utilized to characterize the swallowing function of TPH2 knockout ( TPH2-/-) mice as compared with littermate controls ( TPH2+/+). Results showed that 5-HT deficiency altered all 3 stages of swallowing. As compared with controls, TPH2-/- mice had significantly slower lick and swallow rates and faster esophageal transit times. Future studies with this model are necessary to determine if 5-HT replacement may rescue abnormal swallowing function. If so, supplemental 5-HT therapy may have vast applications for a large population of patients with a variety of neurologic disorders resulting in life-diminishing dysphagia, particularly amyotrophic lateral sclerosis and Parkinson’s disease, for which 5-HT deficiency is implicated in the disease pathogenesis.
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Fagg, Graham E. "l-Glutamate, excitatory amino acid receptors and brain function." Trends in Neurosciences 8 (January 1985): 207–10. http://dx.doi.org/10.1016/0166-2236(85)90080-3.
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Fernstrom, John D. "Monosodium Glutamate in the Diet Does Not Raise Brain Glutamate Concentrations or Disrupt Brain Functions." Annals of Nutrition and Metabolism 73, Suppl. 5 (2018): 43–52. http://dx.doi.org/10.1159/000494782.
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The non-essential amino acid glutamate participates in numerous metabolic pathways in the body. It also performs important physiologic functions, which include a sensory role as one of the basic tastes (as monosodium glutamate [MSG]), and a role in neuronal function as the dominant excitatory neurotransmitter in the central nervous system. Its pleasant taste (as MSG) has led to its inclusion as a flavoring agent in foods for centuries. Glutamate’s neurotransmitter role was discovered only in the last 60 years. Its inclusion in foods has necessitated its safety evaluation, which has raised concerns about its transfer into the blood ultimately increasing brain glutamate levels, thereby causing functional disruptions because it is a neurotransmitter. This concern, originally raised almost 50 years ago, has led to an extensive series of scientific studies to examine this issue, conducted primarily in rodents, non-human primates, and humans. The key findings have been that (a) the ingestion of MSG in the diet does not produce appreciable increases in glutamate concentrations in blood, except when given experimentally in amounts vastly in excess of normal intake levels; and (b) the blood-brain barrier effectively restricts the passage of glutamate from the blood into the brain, such that brain glutamate levels only rise when blood glutamate concentrations are raised experimentally via non-physiologic means. These and related discoveries explain why the ingestion of MSG in the diet does not lead to an increase in brain glutamate concentrations, and thus does not produce functional disruptions in brain. This article briefly summarizes key experimental findings that evaluate whether MSG in the diet poses a threat to brain function.
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Young, A. H., J. H. Hughes, and C. H. Ashton. "Brain 5-HT function in bipolar affective disorder." Acta Neuropsychiatrica 12, no. 3 (September 2000): 91–95. http://dx.doi.org/10.1017/s0924270800035481.
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ABSTRACTBackground: Previous studies suggest that brain serotonin neurotransmission may mediate the actions of lithium carbonate. Acute tryptophan depletion (ATD) reduces brain serotonin and allows the study of this neurotransmitter in patient groups. Serotonin modulates electroencephalographic (EEG) activity, which is abnormal in bipolar disorder, and EEG abnormalities persist in euthymic bipolar patients. The EEG may therefore be a sensitive marker of 5-HT function in bipolar disorder.Aims: This study examined the effects of ATD on mood, suicidal ideation and EEG activity in bipolar patients who were symptomatically stable on lithium.Methods: 19 subjects satisfying DSM-IV criteria for bipolar I disorder participated in a within-subject, double-blind, placebo-controlled random-order crossover study. Following acute tryptophan depletion (induced by a 100g amino acid drink following an overnight fast) symptoms were evaluated, quantitative power spectrum brain mapping and measurement of auditory evoked potentials were carried out.Results: ATD produced a significant fall in the amplitude of N1P2 and P300 components of the auditory evoked potential, but no significant changes in the power spectrum. There was an 83% reduction in plasma tryptophan (p<0.05, paired t-test) after the depleting but not the control drink. No significant changes in mood or suicidally scores were recorded after ATD.Conclusions: ATD attenuates auditory evoked potentials in bipolar disorder but does not reverse lithium's effects on mood and suicidally in bipolar disorder.
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Kugaya, Akira, and Gerard Sanacora. "Beyond Monoamines: Glutamatergic Function in Mood Disorders." CNS Spectrums 10, no. 10 (October 2005): 808–19. http://dx.doi.org/10.1017/s1092852900010403.
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AbstractThe monoamine theory has implicated abnormalities in serotonin and norepinephrine in the pathophysiology of major depression and bipolar illness and contributed greatly to our understanding of mood disorders and their treatment. Nevertheless, some limitations of this model still exist that require researchers and clinicians to seek further explanation and develop novel interventions that reach beyond the confines of the monoaminergic systems. Recent studies have provided strong evidence that glutamate and other amino acid neurotransmitters are involved in the pathophysiology and treatment of mood disorders. Studies employing in vivo magnetic resonance spectroscopy have revealed altered cortical glutamate levels in depressed subjects. Consistent with a model of excessive glutamate-induced excitation in mood disorders, several antiglutamatergic agents, such as riluzole and lamotrigine, have demonstrated potential antidepressant efficacy. Glial cell abnormalities commonly associated with mood disorders may at least partly account for the impairment in glutamate action since glial cells play a primary role in synaptic glutamate removal. A hypothetical model of altered glutamatergic function in mood disorders is proposed in conjunction with potential antidepressant mechanisms of antiglutamatergic agents. Further studies elucidating the role of the glutamatergic system in the pathophysiology of mood and anxiety disorders and studies exploring the efficacy and mechanism of action of antiglutamatergic agents in these disorders, are likely to provide new targets for the development of novel antidepressant agents.
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Nikolova, Yuliya S., Karestan C. Koenen, Sandro Galea, Chiou-Miin Wang, Marianne L. Seney, Etienne Sibille, Douglas E. Williamson, and Ahmad R. Hariri. "Beyond genotype: serotonin transporter epigenetic modification predicts human brain function." Nature Neuroscience 17, no. 9 (August 3, 2014): 1153–55. http://dx.doi.org/10.1038/nn.3778.
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Sharpe, M., K. Hawton, A. Clements, and P. Cowen. "Increased brain serotonin function in men with chronic fatigue syndrome." BMJ 315, no. 7101 (July 19, 1997): 164–65. http://dx.doi.org/10.1136/bmj.315.7101.164.
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Stahl, Stephen M. "Dextromethorphan-quinidine–responsive pseudobulbar affect (PBA): psychopharmacological model for wide-ranging disorders of emotional expression?" CNS Spectrums 21, no. 6 (November 18, 2016): 419–23. http://dx.doi.org/10.1017/s1092852916000742.
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The symptoms of emotional dysregulation associated with the syndrome known as pseudobulbar affect (PBA) can be effectively treated by the sigma, glutamate, and serotonergic agent dextromethorphan combined with quinidine. If the same brain circuits affected in PBA are also compromised in related disorders of emotional expression, dextromethorphan-quinidine and other novel sigma-glutamate-serotonin agents could prove to be novel psychopharmacologic treatments for these conditions as well.