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Van Gompel, Jamie J., Su-Youne Chang, Stephan J. Goerss, In Yong Kim, Christopher Kimble, Kevin E. Bennet, and Kendall H. Lee. "Development of intraoperative electrochemical detection: wireless instantaneous neurochemical concentration sensor for deep brain stimulation feedback." Neurosurgical Focus 29, no. 2 (August 2010): E6. http://dx.doi.org/10.3171/2010.5.focus10110.
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Deep brain stimulation (DBS) is effective when there appears to be a distortion in the complex neurochemical circuitry of the brain. Currently, the mechanism of DBS is incompletely understood; however, it has been hypothesized that DBS evokes release of neurochemicals. Well-established chemical detection systems such as microdialysis and mass spectrometry are impractical if one is assessing changes that are happening on a second-to-second time scale or for chronically used implanted recordings, as would be required for DBS feedback. Electrochemical detection techniques such as fast-scan cyclic voltammetry (FSCV) and amperometry have until recently remained in the realm of basic science; however, it is enticing to apply these powerful recording technologies to clinical and translational applications. The Wireless Instantaneous Neurochemical Concentration Sensor (WINCS) currently is a research device designed for human use capable of in vivo FSCV and amperometry, sampling at subsecond time resolution. In this paper, the authors review recent advances in this electrochemical application to DBS technologies. The WINCS can detect dopamine, adenosine, and serotonin by FSCV. For example, FSCV is capable of detecting dopamine in the caudate evoked by stimulation of the subthalamic nucleus/substantia nigra in pig and rat models of DBS. It is further capable of detecting dopamine by amperometry and, when used with enzyme linked sensors, both glutamate and adenosine. In conclusion, WINCS is a highly versatile instrument that allows near real-time (millisecond) detection of neurochemicals important to DBS research. In the future, the neurochemical changes detected using WINCS may be important as surrogate markers for proper DBS placement as well as the sensor component for a “smart” DBS system with electrochemical feedback that allows automatic modulation of stimulation parameters. Current work is under way to establish WINCS use in humans.
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Paolo, Thérèse Di, Claude Rouillard, Marc Morissette, Daniel Lévesque, and Paul J. Bédard. "Endocrine and neurochemical actions of cocaine." Canadian Journal of Physiology and Pharmacology 67, no. 9 (September 1, 1989): 1177–81. http://dx.doi.org/10.1139/y89-187.
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The endocrine and neurochemical actions of cocaine in human and animal studies are reviewed. In humans, cocaine has been shown to influence plasma prolactin and growth hormone, as well as the dexamethasone suppression of cortisol and the thyroid-stimulating hormone response to thyroid-releasing hormone. In rats, cocaine affects plasma prolactin, luteinizing hormone, and testosterone, and can lead to adrenocortical hypertrophy. Behavioral sensitization to cocaine in rats has been shown to be related to the gender of the animals and appears to be modulated by vasopressin. A review of the neurochemical actions of cocaine indicates the important role of dopamine systems in the euphoric effects of the drug, as well as its withdrawal symptoms. Cocaine is a potent dopamine uptake inhibitor, as shown by its competition with [3H]GBR-12935 (a specific ligand for the dopamine uptake sites) for striatum binding sites. However, it does not acutely affect the high-affinity agonist sites of the D-2 dopamine receptors, which are suggested to be the active form of the presynaptic receptor. Using microdialysis techniques, cocaine is shown to rapidly cause a large increase of rat striatal dopamine levels, while its metabolites dihydroxyphenylacetic acid and homovanillic acid are slightly decreased and increased, respectively.Key words: cocaine, dopamine, hormones, neurochemistry, microdialysis.
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Chang, An-Yi, Shabnam Siddiqui, and Prabhu U. Arumugam. "Nafion and Multiwall Carbon Nanotube Modified Ultrananocrystalline Diamond Microelectrodes for Detection of Dopamine and Serotonin." Micromachines 12, no. 5 (May 6, 2021): 523. http://dx.doi.org/10.3390/mi12050523.
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Neurochemicals play a critical role in the function of the human brain in healthy and diseased states. Here, we have investigated three types of microelectrodes, namely boron-doped ultrananocrystalline diamond (BDUNCD), nafion-modified BDUNCD, and nafion–multi-walled carbon nanotube (MWCNT)-modified BDUNCD microelectrodes for long-term neurochemical detection. A ~50 nm-thick nafion–200-nm-thick MWCNT-modified BDUNCD microelectrode provided an excellent combination of sensitivity and selectivity for the detection of dopamine (DA; 6.75 μA μM−1 cm−2) and serotonin (5-HT; 4.55 μA μM−1 cm−2) in the presence of excess amounts of ascorbic acid (AA), the most common interferent. Surface stability studies employing droplet-based microfluidics demonstrate rapid response time (<2 s) and low limits of detection (5.4 ± 0.40 nM). Furthermore, we observed distinguishable DA and 5-HT current peaks in a ternary mixture during long-term stability studies (up to 9 h) with nafion–MWCNT-modified BDUNCD microelectrodes. Reduced fouling on the modified BDUNCD microelectrode surface offers significant advantages for their use in long-term neurochemical detection as compared to those of prior-art microelectrodes.
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Critz, Stuart D., and Robert E. Marc. "Glutamate antagonists that block hyperpolarizing bipolar cells increase the release of dopamine from turtle retina." Visual Neuroscience 9, no. 3-4 (October 1992): 271–78. http://dx.doi.org/10.1017/s0952523800010683.
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AbstractSome neurochemical features of the neuronal circuitry regulating dopamine release were examined in the retina of the turtle, Pseudemys scripta elegans. Glutamate antagonists that block hyperpolarizing bipolar cells, such as 2,3 piperidine dicarboxylic acid (PDA), produced dose-dependent dopamine release. In contrast, the glutamate agonist 2-amino-4-phosphonobutyric acid (APB), which blocks depolarizing bipolar cell responses with high specificity, had no effect on the release of dopamine. The γ-aminobutyric acid (GABA) antagonist, bicuculline, also produced potent dose-dependent release of dopamine. The release of dopamine produced by PDA was blocked by exogenous GABA and muscimol, suggesting that the PDA-mediated release process was polysynaptic and involved a GABAergic synapse interposed between the bipolar and dopaminergic amacrine cells. The only other agents that produced dopamine release were chloride-free media and high extracellular K+; in particular, kainic acid and glutamate itself were ineffective. These results suggest that the primary neuronal chain mediating dopamine release in the turtle retina is: cone → hyperpolarizing bipolar cell → GABAergic amacrine cell → dopaminergic amacrine cell.
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Izenwasser, S. "Is dopamine the answer? Other systems in the neurochemical effects of psychostimulants." Journal of Neurochemistry 81 (June 28, 2008): 39. http://dx.doi.org/10.1046/j.1471-4159.2002.00084.x.
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Reynolds, G. P. "Beyond the Dopamine Hypothesis." British Journal of Psychiatry 155, no. 3 (September 1989): 305–16. http://dx.doi.org/10.1192/bjp.155.3.305.
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The dopamine hypothesis still provides a valuable approach to the study of schizophrenia and its treatment by drugs. Although the neuroleptic drugs appear to act via an inhibition of dopamine receptors, measurements of dopamine metabolites in vivo, or of the transmitter and its receptors in postmortem brain tissue, do not provide unequivocal evidence of a hyperactivity of dopaminergic neurotransmission in the disease. Nevertheless, increased dopamine function might be a consequence of a primary neuronal abnormality in another system. Recent imaging studies and neuropathological reports suggest that, in some patients, there may be a deficit and/or disturbance of neurons in certain temporal limbic regions, and this is supported by some neurochemical investigations, particularly of neuropeptide and amino-acid transmitter systems. A loss of such neurons could conceivably lead to a disinhibition of limbic dopamine neurons, providing the means whereby neuroleptic drug treatment might ameliorate the effects of a neuronal deficit in schizophrenia.
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Dust, Julian M. "Charge transfer and electron transfer processes in biologically significant systems. 1. Charge transfer complex formation between 1,3,5-trinitrobenzene and N,N-dimethyl-3,4-di-O-methyldopamine, a dopamine analogue." Canadian Journal of Chemistry 70, no. 1 (January 1, 1992): 151–57. http://dx.doi.org/10.1139/v92-025.
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The interactions of N,N-dimethyl-3,4-di-O-methyldopamine, 1, a structural analogue of the important neurochemical, dopamine, with 1,3,5-trinitrobenzene (TNB) were studied primarily by 1H nuclear magnetic resonance (nmr). The dopamine analogue, a donor, forms a charge transfer complex with TNB, a model acceptor, in CDCl3 and CD3CN. Equilibrium constants were determined from the 1H nmr charge transfer induced chemical shift changes. The results are discussed in terms of the probable type of donation from the amine, 1, to TNB (n → π* versus π → π*), comparison with dopamine, and with regard to possible charge transfer interactions in molecular receptors. Keywords: N,N-dimethyl-3,4-di-O-methyldopamine, charge transfer complex, equilibrium constant.
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Bledsoe, Jonathan M., Christopher J. Kimble, Daniel P. Covey, Charles D. Blaha, Filippo Agnesi, Pedram Mohseni, Sidney Whitlock, et al. "Development of the Wireless Instantaneous Neurotransmitter Concentration System for intraoperative neurochemical monitoring using fast-scan cyclic voltammetry." Journal of Neurosurgery 111, no. 4 (October 2009): 712–23. http://dx.doi.org/10.3171/2009.3.jns081348.
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Object Emerging evidence supports the hypothesis that modulation of specific central neuronal systems contributes to the clinical efficacy of deep brain stimulation (DBS) and motor cortex stimulation (MCS). Real-time monitoring of the neurochemical output of targeted regions may therefore advance functional neurosurgery by, among other goals, providing a strategy for investigation of mechanisms, identification of new candidate neurotransmitters, and chemically guided placement of the stimulating electrode. The authors report the development of a device called the Wireless Instantaneous Neurotransmitter Concentration System (WINCS) for intraoperative neurochemical monitoring during functional neurosurgery. This device supports fast-scan cyclic voltammetry (FSCV) at a carbon-fiber microelectrode (CFM) for real-time, spatially and chemically resolved neurotransmitter measurements in the brain. Methods The FSCV study consisted of a triangle wave scanned between −0.4 and 1 V at a rate of 300 V/second and applied at 10 Hz. All voltages were compared with an Ag/AgCl reference electrode. The CFM was constructed by aspirating a single carbon fiber (r = 2.5 μm) into a glass capillary and pulling the capillary to a microscopic tip by using a pipette puller. The exposed carbon fiber (that is, the sensing region) extended beyond the glass insulation by ~ 100 μm. The neurotransmitter dopamine was selected as the analyte for most trials. Proof-of-principle tests included in vitro flow injection and noise analysis, and in vivo measurements in urethane-anesthetized rats by monitoring dopamine release in the striatum following high-frequency electrical stimulation of the medial forebrain bundle. Direct comparisons were made to a conventional hardwired system. Results The WINCS, designed in compliance with FDA-recognized consensus standards for medical electrical device safety, consisted of 4 modules: 1) front-end analog circuit for FSCV (that is, current-to-voltage transducer); 2) Bluetooth transceiver; 3) microprocessor; and 4) direct-current battery. A Windows-XP laptop computer running custom software and equipped with a Universal Serial Bus–connected Bluetooth transceiver served as the base station. Computer software directed wireless data acquisition at 100 kilosamples/second and remote control of FSCV operation and adjustable waveform parameters. The WINCS provided reliable, high-fidelity measurements of dopamine and other neurochemicals such as serotonin, norepinephrine, and ascorbic acid by using FSCV at CFM and by flow injection analysis. In rats, the WINCS detected subsecond striatal dopamine release at the implanted sensor during high-frequency stimulation of ascending dopaminergic fibers. Overall, in vitro and in vivo testing demonstrated comparable signals to a conventional hardwired electrochemical system for FSCV. Importantly, the WINCS reduced susceptibility to electromagnetic noise typically found in an operating room setting. Conclusions Taken together, these results demonstrate that the WINCS is well suited for intraoperative neurochemical monitoring. It is anticipated that neurotransmitter measurements at an implanted chemical sensor will prove useful for advancing functional neurosurgery.
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Koob, George F., and Michel Le Moal. "Neurobiological mechanisms for opponent motivational processes in addiction." Philosophical Transactions of the Royal Society B: Biological Sciences 363, no. 1507 (July 24, 2008): 3113–23. http://dx.doi.org/10.1098/rstb.2008.0094.
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The conceptualization of drug addiction as a compulsive disorder with excessive drug intake and loss of control over intake requires motivational mechanisms. Opponent process as a motivational theory for the negative reinforcement of drug dependence has long required a neurobiological explanation. Key neurochemical elements involved in reward and stress within basal forebrain structures involving the ventral striatum and extended amygdala are hypothesized to be dysregulated in addiction to convey the opponent motivational processes that drive dependence. Specific neurochemical elements in these structures include not only decreases in reward neurotransmission such as dopamine and opioid peptides in the ventral striatum, but also recruitment of brain stress systems such as corticotropin-releasing factor (CRF), noradrenaline and dynorphin in the extended amygdala. Acute withdrawal from all major drugs of abuse produces increases in reward thresholds, anxiety-like responses and extracellular levels of CRF in the central nucleus of the amygdala. CRF receptor antagonists block excessive drug intake produced by dependence. A brain stress response system is hypothesized to be activated by acute excessive drug intake, to be sensitized during repeated withdrawal, to persist into protracted abstinence and to contribute to stress-induced relapse. The combination of loss of reward function and recruitment of brain stress systems provides a powerful neurochemical basis for the long hypothesized opponent motivational processes responsible for the negative reinforcement driving addiction.
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Salvatore, Michael F., Brent Fisher, Stewart P. Surgener, Greg A. Gerhardt, and Tracey Rouault. "Neurochemical investigations of dopamine neuronal systems in iron-regulatory protein 2 (IRP-2) knockout mice." Molecular Brain Research 139, no. 2 (October 2005): 341–47. http://dx.doi.org/10.1016/j.molbrainres.2005.06.002.
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Liang, Yuanying, Ting Guo, Lei Zhou, Andreas Offenhäusser, and Dirk Mayer. "Label-Free Split Aptamer Sensor for Femtomolar Detection of Dopamine by Means of Flexible Organic Electrochemical Transistors." Materials 13, no. 11 (June 5, 2020): 2577. http://dx.doi.org/10.3390/ma13112577.
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The detection of chemical messenger molecules, such as neurotransmitters in nervous systems, demands high sensitivity to measure small variations, selectivity to eliminate interferences from analogues, and compliant devices to be minimally invasive to soft tissue. Here, an organic electrochemical transistor (OECT) embedded in a flexible polyimide substrate is utilized as transducer to realize a highly sensitive dopamine aptasensor. A split aptamer is tethered to a gold gate electrode and the analyte binding can be detected optionally either via an amperometric or a potentiometric transducer principle. The amperometric sensor can detect dopamine with a limit of detection of 1 μM, while the novel flexible OECT-based biosensor exhibits an ultralow detection limit down to the concentration of 0.5 fM, which is lower than all previously reported electrochemical sensors for dopamine detection. The low detection limit can be attributed to the intrinsic amplification properties of OECTs. Furthermore, a significant response to dopamine inputs among interfering analogues hallmarks the selective detection capabilities of this sensor. The high sensitivity and selectivity, as well as the flexible properties of the OECT-based aptasensor, are promising features for their integration in neuronal probes for the in vitro or in vivo detection of neurochemical signals.
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Schwarz, Aline, Rosana Zoriki Hosomi, Jorge Camilo Flório, Maria Martha Bernardi, Silvana Lima Górniak, and Helenice Souza Spinosa. "Rats offspring exposed to Ipomoea Carnea and handling during gestation: neurochemical evaluation." Brazilian Archives of Biology and Technology 50, no. 3 (May 2007): 425–33. http://dx.doi.org/10.1590/s1516-89132007000300009.
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The present study evaluated the central monoamine levels of male and female adult rat offspring exposed orally by gavage to 0.0, 0.7, 3.0 and 15.0 mg/kg I. carnea aqueous extract daily, from gestation day (GD) 5 to GD 21. Several alterations in the monoamine activity systems were observed. However, the major differences were noted between the 0.0 mg/kg and the no gavage control groups, showing that alterations showing that alterations were not due to the alterations to the aqueous extract. The control data showed that gavage and handling of dams were stressful enough to produce a significant decline in 3,4-dihydroxyphenylacetic acid (DOPAC) and an increase in vanilmandelic acid (VMA), indicating decreased dopamine (DA) and enhanced norepinephrine (NE) activity, respectively.
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Rojas Cabrera, Juan M., J. Blair Price, Aaron E. Rusheen, Abhinav Goyal, Danielle Jondal, Abhijeet S. Barath, Hojin Shin, et al. "Advances in neurochemical measurements: A review of biomarkers and devices for the development of closed-loop deep brain stimulation systems." Reviews in Analytical Chemistry 39, no. 1 (January 1, 2020): 188–99. http://dx.doi.org/10.1515/revac-2020-0117.
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Abstract Neurochemical recording techniques have expanded our understanding of the pathophysiology of neurological disorders, as well as the mechanisms of action of treatment modalities like deep brain stimulation (DBS). DBS is used to treat diseases such as Parkinson’s disease, Tourette syndrome, and obsessive-compulsive disorder, among others. Although DBS is effective at alleviating symptoms related to these diseases and improving the quality of life of these patients, the mechanism of action of DBS is currently not fully understood. A leading hypothesis is that DBS modulates the electrical field potential by modifying neuronal firing frequencies to non-pathological rates thus providing therapeutic relief. To address this gap in knowledge, recent advances in electrochemical sensing techniques have given insight into the importance of neurotransmitters, such as dopamine, serotonin, glutamate, and adenosine, in disease pathophysiology. These studies have also highlighted their potential use in tandem with electrophysiology to serve as biomarkers in disease diagnosis and progression monitoring, as well as characterize response to treatment. Here, we provide an overview of disease-relevant neurotransmitters and their roles and implications as biomarkers, as well as innovations to the biosensors used to record these biomarkers. Furthermore, we discuss currently available neurochemical and electrophysiological recording devices, and discuss their viability to be implemented into the development of a closed-loop DBS system.
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Yang, Chae Ha, Bong Hyo Lee, and Sung Hoon Sohn. "A Possible Mechanism Underlying the Effectiveness of Acupuncture in the Treatment of Drug Addiction." Evidence-Based Complementary and Alternative Medicine 5, no. 3 (2008): 257–66. http://dx.doi.org/10.1093/ecam/nem081.
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Clinical trials are currently underway to determine the effectiveness of acupuncture in the treatment of drug addiction. While there are still many unanswered questions about the basic mechanisms of acupuncture, some evidence exists to suggest that acupuncture can play an important role in reducing reinforcing effects of abused drugs. The purpose of this article is to critically review these data. The neurochemical and behavioral evidence showed that acupuncture's role in suppressing the reinforcing effects of abused drugs takes place by modulating mesolimbic dopamine neurons. Also, several brain neurotransmitter systems such as serotonin, opioid and amino acids including GABA have been implicated in the modulation of dopamine release by acupuncture. These results provided clear evidence for the biological effects of acupuncture that ultimately may help us to understand how acupuncture can be used to treat abused drugs. Additional research using animal models is of primary importance to understanding the basic mechanism underlying acupuncture's effectiveness in the treatment of drug addiction.
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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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SÁNCHEZ-CAMACHO, CRISTINA, OSCAR MARÍN, and AGUSTÍN GONZÁLEZ. "Distribution and origin of the catecholaminergic innervation in the amphibian mesencephalic tectum." Visual Neuroscience 19, no. 3 (May 2002): 321–33. http://dx.doi.org/10.1017/s0952523802192091.
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The mesencephalic tectum plays a prominent role in integrating both visual and multimodal sensory information essential for normal behavior in amphibians. Activity in the mesencephalic tectum is thought to be modulated by the influence of distinct neurochemical inputs, including the catecholaminergic and the cholinergic systems. In the present study, we have investigated the distribution and the origin of the catecholaminergic innervation of the mesencephalic tectum in two amphibian species, the anuran Rana perezi and the urodele Pleurodeles waltl. Immunohistochemistry for dopamine and two enzymes required for the synthesis of catecholamines, tyrosine hydroxylase (TH) and dopamine β-hydroxylase (DBH), revealed a complex pattern of catecholaminergic (CA) innervation in the anuran and urodele mesencephalic tectum. Dopaminergic fibers were primarily present in deep tectal layers, whereas noradrenergic (DBH immunoreactive) fibers predominated in superficial layers. Catecholaminergic cell bodies were never observed within the tectum. To determine the origin of this innervation, applications of retrograde tracers into the optic tectum were combined with immunohistochemistry for TH. Results from these experiments demonstrate that dopaminergic neurons in the suprachiasmatic and juxtacommissural nuclei (in Rana) or in the nucleus pretectalis (in Pleurodeles), together with noradrenergic cells of the locus coeruleus, are the sources of CA input to the amphibian mesencephalic tectum. The present results suggest that similar CA modulatory inputs are present in the mesecencephalic tectum of both anurans and urodeles.
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Koob, George F., and Amanda J. Roberts. "Brain Reward Circuits in Alcoholism." CNS Spectrums 4, no. 1 (January 1999): 23–37. http://dx.doi.org/10.1017/s1092852900011196.
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AbstractThis article discusses the neurocircuitry and the neurochemical systems, as well as the molecular elements within these systems, that are believed to be important in the etiology of alcoholism. Alcoholism is a complex behavioral disorder characterized by excessive consumption of alcohol; a narrowing of the behavioral repertoire toward excessive consumption; the development of tolerance and dependence; and impairment in social and occupational functioning. Animal models of the complete syndrome of alcoholism are difficult if not impossible to achieve, but validated animal models exist for many of the different components of the syndrome.Recent work has begun to define the neurocircuits responsible for the major sources of positive and negative reinforcement that are key to animal models of excessive alcohol intake. Alcohol appears to interact with alcohol-sensitive elements within neuronal membranes that convey the specificity of neurochemical actions. Positive reinforcement appears to be mediated by an activation γ-aminobutyric acid A receptors, release of opioid peptides and dopamine, inhibition of glutamate receptors, and interaction with serotonin systems. These neurocircuits may be altered by chronic alcohol administration. This is reflected by their exhibiting opposite effects during acute alcohol withdrawal, and by the recruitment of other neurotransmitter systems, such as the stress neuropeptide corticotropin-releasing factor. These neuropharmacologic actions are believed to produce allostatic changes in set-point, which set up the vulnerability to relapse that is so characteristic of alcoholism. Future challenges include a focus on understanding exactly how these neuroadaptive changes convey vulnerability to relapse in animals with a history of alcohol dependence.
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Antunes, Geiza Fernanda, Flavia Venetucci Gouveia, Fabiana Strambio Rezende, Midiã Dias de Jesus Seno, Milene Cristina de Carvalho, Caroline Cruz de Oliveira, Lennon Cardoso Tosati dos Santos, et al. "Dopamine modulates individual differences in avoidance behavior: A pharmacological, immunohistochemical, neurochemical and volumetric investigation." Neurobiology of Stress 12 (May 2020): 100219. http://dx.doi.org/10.1016/j.ynstr.2020.100219.
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Short, Jennifer Lynn, John Drago, and Andrew John Lawrence. "Comparison of Ethanol Preference and Neurochemical Measures of Mesolimbic Dopamine and Adenosine Systems Across Different Strains of Mice." Alcoholism: Clinical and Experimental Research 30, no. 4 (April 2006): 606–20. http://dx.doi.org/10.1111/j.1530-0277.2006.00071.x.
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Amat, Nurmuhammat, Parida Hoxur, Dang Ming, Aynur Matsidik, Anake Kijjoa, and Halmurat Upur. "Behavioral, Neurochemical and Neuroendocrine Effects of Abnormal Savda Munziq in the Chronic Stress Mice." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/426757.
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Oral administration of Abnormal Savda Munsiq (ASMq), a herbal preparation used in Traditional Uighur Medicine, was found to exert a memory-enhancing effect in the chronic stressed mice, induced by electric foot-shock. The memory improvement of the stressed mice was shown by an increase of the latency time in the step-through test and the decrease of the latency time in the Y-maze test. Treatment with ASMq was found to significantly decrease the serum levels of adrenocorticotropic hormone (ACTH), corticosterone (CORT) and -endorphin (-EP) as well as the brain and serum level of norepinephrine (NE). Furthermore, ASMq was able to significantly reverse the chronic stress by decreasing the brain and serum levels of the monoamine neurotransmitters dopamine (DA), 5-hydroxytryptamine (5-HT) and 3,4-dihydroxyphenylalanine (DOPAC). The results obtained from this study suggested that the memory-enhancing effect of ASMq was mediated through regulations of neurochemical and neuroendocrine systems.
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Trofimova, I. "Integrating the Findings from Boundary Sciences for Development of the DSM/ICD Classifications." European Psychiatry 41, S1 (April 2017): S78. http://dx.doi.org/10.1016/j.eurpsy.2017.01.249.
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IntroductionTemperament and mental illnesses are considered to be varying degrees along the same continuum of imbalance in the neurophysiological regulation of behavior. Mental disorders are linked to specific patterns in the relationships between neurotransmitters and between brain structures. Similar links were found for temperament traits. Development of DSM and ICD classifications might benefit therefore from an integration between psychiatry, functional neurochemistry and differential psychology.ObjectivesTo describe the neurochemical systems underlying mental disorders and temperament traits in healthy adults.MethodsFindings in neurochemistry, neuropsychology, differential psychology and psychopathology are compared to the traits described in various temperament models. This analysis is summarized in the perspective of the neurochemical functional ensemble of temperament (FET) model.ResultsNeurochemical correlates for 12 main dynamical aspects of behavior are presented as a systemic framework that follows a universal functional structure of human actions described in kinesiology, neuroanatomy, neurochemistry and clinical neuropsychology. The role of monoamine systems (serotonin, dopamine, noradrenalin), acetylcholine, GABA/glutamate, neuropeptide and opioid receptor systems are linked to regulation of specific dynamical properties of behavior in a systematic way. Several insights for the structure of the classification of mental disorders from the perspective of the FET model are proposed.ConclusionsAn integration of research in neurochemistry and psychopathology of behavior with differential psychology based on healthy samples can bring new insights for future versions of DSM and ICD classifications of mental disorders. Such integration does not follow either dimensionality or categorical approach but instead is based on functional ecology of human behavior.Disclosure of interestThe author has not supplied his declaration of competing interest.
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Manta, Stella, Mostafa El Mansari, Guy Debonnel, and Pierre Blier. "Electrophysiological and neurochemical effects of long-term vagus nerve stimulation on the rat monoaminergic systems." International Journal of Neuropsychopharmacology 16, no. 2 (April 17, 2012): 459–70. http://dx.doi.org/10.1017/s1461145712000387.
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Abstract Vagus nerve stimulation (VNS) is an adjunctive treatment for resistant epilepsy and depression. Electrophysiological recordings in the rat brain have already shown that chronic VNS increases norepinephrine (NE) neuronal firing activity and, subsequently, that of serotonin (5-HT) neurons through an activation of their excitatory α1-adrenoceptors. Long-term VNS was shown to increase the tonic activation of post-synaptic 5-HT1A receptors in the hippocampus. This study was aimed at examining the effect of VNS on extracellular 5-HT, NE and dopamine (DA) levels in different brain areas using in vivo microdialysis, on NE transmission in the hippocampus, and DA neuronal firing activity using electrophysiology. Rats were implanted with a VNS device and stimulated for 14 d with standard parameters used in treatment-resistant depression (0.25 mA, 20 Hz, 500 µs, 30 s on–5 min off). The results of the present study revealed that 2-wk VNS significantly increased extracellular NE levels in the prefrontal cortex and the hippocampus and enhanced the tonic activation of post-synaptic α2-adrenoceptors on pyramidal neurons. The electrophysiological experiments revealed a significant decrease in ventral tegmental area DA neuronal firing rate after long-term VNS; extracellular DA levels were nevertheless increased in the prefrontal cortex and nucleus accumbens. Chronic VNS significantly increased extracellular 5-HT levels in the dorsal raphe but not in the hippocampus and prefrontal cortex. In conclusion, the effect of VNS in increasing the transmission of monoaminergic systems targeted in the treatment of resistant depression should be involved, at least in part, in its antidepressant properties observed in patients not responding to many antidepressant strategies.
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Gopalan, Chaya, Ye Tian, Kenneth E. Moore, and Keith J. Lookingland. "Neurochemical Evidence that the Inhibitory Effect of Galanin on Tuberoinfundibular Dopamine Neurons Is Activity Dependent." Neuroendocrinology 58, no. 3 (1993): 287–93. http://dx.doi.org/10.1159/000126552.
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Kiefer, F., and K. Mann. "Recent Developments in Decoding Neurobiological Pathways and Treatment Targets in Alcohol Dependence." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70251-2.
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Multiple neurochemical pathways have been identified to be involved in mediating craving and relapse to alcohol and, further, animal models greatly assist in investigating pharmacological interventions of relapse behaviour. Opioidergic and glutamatergic systems play a key role in alcoholism as demonstrated by the clinically effective compounds naltrexone and acamprosate acting through these systems. Although the dopaminergic system has been in the focus of alcohol research for many years, clinical trials interfering with several components of this system displayed rather disappointing results. This situation, however, could change in light of the discovery that dopamine D3 receptor antagonism produces very consistent and robust results in preclinical studies. Corticotropin-releasing factor signalling and the endocannabinoid system integrate stress-related events and thereby mediate relapse behaviour. Thus, many new targets have been identified and several new compounds are currently undergoing clinical testing. However, given the heterogeneity in treatment response, genetic and protein markers as well as endophenotypes are currently characterised for individualised pharmacotherapy.
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Kopp, Darin A., Sonya M. Bierbower, Alexandrea D. Murphy, Kimberly Mormann, and Timothy C. Sparkes. "Parasite-related modification of mating behaviour and refuge use in the aquatic isopod Caecidotea intermedius: neurological correlates." Behaviour 153, no. 8 (2016): 947–61. http://dx.doi.org/10.1163/1568539x-00003379.
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The acanthocephalan Acanthocephalus dirus is a trophically transmitted parasite that infects freshwater isopods as intermediate hosts and fish as definitive hosts. Using a laboratory-based experiment, we examined if parasite infection was associated with changes in mating behaviour, refuge use and neurochemical levels of infected isopods (Caecidotea intermedius). Infected isopods were less likely to engage in mating behaviour and more likely to be located in the open than uninfected isopods. Infected isopods also contained lower levels of serotonin (5-HT) and dopamine (DA) and had a greater mass of neural tissue (CNS) than uninfected isopods. We propose that the parasite-related changes in mating behaviour and refuge use may be modulated by the serotonergic and dopaminergic systems. We also suggest that the parasites could potentially be modulating these behavioural changes by exploiting the neural-immune system of the hosts through their neuroinflammatory responses.
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Zhu, Yunqi, Hong Zhang, and Mei Tian. "Molecular and Functional Imaging of Internet Addiction." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/378675.
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Maladaptive use of the Internet results in Internet addiction (IA), which is associated with various negative consequences. Molecular and functional imaging techniques have been increasingly used for analysis of neurobiological changes and neurochemical correlates of IA. This review summarizes molecular and functional imaging findings on neurobiological mechanisms of IA, focusing on magnetic resonance imaging (MRI) and nuclear imaging modalities including positron emission tomography (PET) and single photon emission computed tomography (SPECT). MRI studies demonstrate that structural changes in frontal cortex are associated with functional abnormalities in Internet addicted subjects. Nuclear imaging findings indicate that IA is associated with dysfunction of the brain dopaminergic systems. Abnormal dopamine regulation of the prefrontal cortex (PFC) could underlie the enhanced motivational value and uncontrolled behavior over Internet overuse in addicted subjects. Further investigations are needed to determine specific changes in the Internet addictive brain, as well as their implications for behavior and cognition.
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Gvirts, Hila Z., and Rotem Perlmutter. "What Guides Us to Neurally and Behaviorally Align With Anyone Specific? A Neurobiological Model Based on fNIRS Hyperscanning Studies." Neuroscientist 26, no. 2 (July 11, 2019): 108–16. http://dx.doi.org/10.1177/1073858419861912.
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An emerging body of hyperscanning functional near-infrared spectroscopy (fNIRS) research shows interbrain neural synchrony (IBS) during different forms of social interaction. Here we review the recent literature and propose several factors that facilitate IBS, leading us to ask the following question: In a world full of people and opportunities to synchronize with them, what directs our neural and behavioral alignment with anyone specific? We suggest that IBS between what we deem the “mutual social attention systems” of interacting partners—that is, the coupling between participants’ temporoparietal junctions and/or prefrontal cortices—facilitates and enhances the ability to tune in to the specific interaction, its participants and its goals. We propose that this process is linked to social alignment, reinforcing one another to facilitate successful and lucrative social interactions. We further suggest that neurochemical mechanisms of dopamine and oxytocin underlie the activation of this suggested loop. Finally, we suggest possible directions for future studies, emphasizing the need to develop a brain-to-brain neurofeedback system with IBS between the mutual social attention systems of the participants as the direct regulating target.
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Arya, Ashwani, Gulshan Sindhwani, and Renu Kadian. "NEUROTRANSMITTER AND BRAIN PARTS INVOLVED IN SCHIZOPHRENIA." Asian Journal of Pharmaceutical and Clinical Research 11, no. 6 (June 7, 2018): 4. http://dx.doi.org/10.22159/ajpcr.2018.v11i6.24557.
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Schizophrenia (SCZ) is a major debilitating, complex, and costly illness that strikes 1% of the world’s population. It is characterized by three general types of symptoms: Atypical symptoms (aggressiveness, agitation, delusions, hallucinations), depressive symptoms (alogia, avolition, anhedonia, apathy), and cognitive symptoms (impaired attention, learning, memory). The etiology of SCZ has still not been fully understood. Alteration in various neurochemical systems such as dopamine, serotonin, norepinephrine, gamma-aminobutyric acid, and glutamate are involved in the pathophysiology of SCZ. The lack of understanding regarding the exact pathogenic process may be the likely a reason for the non-availability of effective treatment, which can prevent onset and progression of the SCZ. The tools of modern neuroscience, drawing from neuroanatomy, neurophysiology, brain imaging, and psychopharmacology, promise to provide a host of new insights into the etiology and treatment of SCZ. In this review, we will discuss the role of the various neurotransmitter concerned and brain parts exaggerated in the SCZ.
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Dalvi-Garcia, Felipe, Luis L. Fonseca, Ana Tereza R. Vasconcelos, Cecilia Hedin-Pereira, and Eberhard O. Voit. "A model of dopamine and serotonin-kynurenine metabolism in cortisolemia: Implications for depression." PLOS Computational Biology 17, no. 5 (May 10, 2021): e1008956. http://dx.doi.org/10.1371/journal.pcbi.1008956.
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A major factor contributing to the etiology of depression is a neurochemical imbalance of the dopaminergic and serotonergic systems, which is caused by persistently high levels of circulating stress hormones. Here, a computational model is proposed to investigate the interplay between dopaminergic and serotonergic-kynurenine metabolism under cortisolemia and its consequences for the onset of depression. The model was formulated as a set of nonlinear ordinary differential equations represented with power-law functions. Parameter values were obtained from experimental data reported in the literature, biological databases, and other general information, and subsequently fine-tuned through optimization. Model simulations predict that changes in the kynurenine pathway, caused by elevated levels of cortisol, can increase the risk of neurotoxicity and lead to increased levels of 3,4-dihydroxyphenylaceltahyde (DOPAL) and 5-hydroxyindoleacetaldehyde (5-HIAL). These aldehydes contribute to alpha-synuclein aggregation and may cause mitochondrial fragmentation. Further model analysis demonstrated that the inhibition of both serotonin transport and kynurenine-3-monooxygenase decreased the levels of DOPAL and 5-HIAL and the neurotoxic risk often associated with depression. The mathematical model was also able to predict a novel role of the dopamine and serotonin metabolites DOPAL and 5-HIAL in the ethiology of depression, which is facilitated through increased cortisol levels. Finally, the model analysis suggests treatment with a combination of inhibitors of serotonin transport and kynurenine-3-monooxygenase as a potentially effective pharmacological strategy to revert the slow-down in monoamine neurotransmission that is often triggered by inflammation.
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Chen, Feng, Amir H. Rezvani, and Andrew J. Lawrence. "Autoradiographic quantification of neurochemical markers of serotonin, dopamine and opioid systems in rat brain mesolimbic regions following chronic St. John's wort treatment." Naunyn-Schmiedeberg's Archives of Pharmacology 367, no. 2 (February 2003): 126–33. http://dx.doi.org/10.1007/s00210-002-0666-3.
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Bharatiya, Rahul, Abdeslam Chagraoui, Salomé De Deurwaerdere, Antonio Argiolas, Maria Rosaria Melis, Fabrizio Sanna, and Philippe De Deurwaerdere. "Chronic Administration of Fipronil Heterogeneously Alters the Neurochemistry of Monoaminergic Systems in the Rat Brain." International Journal of Molecular Sciences 21, no. 16 (August 9, 2020): 5711. http://dx.doi.org/10.3390/ijms21165711.
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Fipronil (FPN), a widely used pesticide for agricultural and non-agricultural pest control, is possibly neurotoxic for mammals. Brain monoaminergic systems, involved in virtually all brain functions, have been shown to be sensitive to numerous pesticides. Here, we addressed the hypothesis that chronic exposure to FPN could modify brain monoamine neurochemistry. FPN (10 mg/kg) was chronically administered for 21 days through oral gavage in rats. Thereafter, the tissue concentrations of dopamine (DA) and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid; serotonin (5-HT) and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA); and noradrenaline (NA) were measured in 30 distinct brain regions. FPN significantly decreased DA and its metabolite levels in most striatal territories, including the nucleus accumbens and the substantia nigra (SN). FPN also diminished 5-HT levels in some striatal regions and the SN. The indirect index of the turnovers, DOPAC/DA and 5-HIAA/5-HT ratios, was increased in numerous brain regions. FPN reduced the NA content only in the nucleus accumbens core. Using the Bravais–Pearson test to study the neurochemical organization of monoamines through multiple correlative analyses across the brain, we found fewer correlations for NA, DOPAC/DA, and 5-HIAA/5-HT ratios, and an altered pattern of correlations within and between monoamine systems. We therefore conclude that the chronic administration of FPN in rats induces massive and inhomogeneous changes in the DA and 5-HT systems in the brain.
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Zubenko, George S. "Neurobiology of Major Depression in Alzheimer's Disease." International Psychogeriatrics 12, S1 (July 2000): 217–30. http://dx.doi.org/10.1017/s1041610200007079.
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The original catecholamine hypothesis of affective disorders focused largely on the role of the noradrenergic components of the central nervous system in the etiology of depression and mania (Bunney & Davis, 1965; Schildkraut, 1965). Additional evidence from clinical, pharmacologic, and physiologic studies has emerged since the original hypothesis was proposed and generally supports the view that clinically significant depression can result from a dysfunction of central nervous system mechanisms employing the catecholamine neurotransmitters norepinephrine and dopamine (Jimerson, 1987; Siever, 1987). Neurochemical studies of serotonin (5-HT) receptors and 5-hydroxyindoleacetic acid (5-HIAA) in spinal fluid or brain tissue also suggest an alteration in serotonergic components of the central nervous system in both idiopathic major depression and suicide (Brikmayer & Riederer, 1975; Crow et al., 1984; Lloyd et al., 1974; Mendlewicz et al., 1981; Stanley & Mann, 1983). In contrast to these hypotheses, which suggest that depression may result from the decreased function of one or more central aminergic systems, the cholinergic hypothesis of affective disorders (Janowsky & Risch, 1987) posits that idiopathic depression is associated with the hyperfunctioning of cholinergic systems. This hypothesis is especially interesting in the context of Alzheimer's disease (AD) because the progression of the central cholinergic deficit that occurs in this disorder may interact with the pathophysiology of depression to limit the prevalence of major depression in later stages of this disorder.
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Rezaei, Shaghayegh, Nour Mohammad Bakhshani, Hamed Fanaei, and Irina Trofimova. "Opium Effect in Pregnancy on the Dynamics of Maternal Behavior: Testing a Neurochemical Model." Neuropsychobiology 80, no. 2 (2021): 147–57. http://dx.doi.org/10.1159/000512698.
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<b><i>Background:</i></b> Investigations into neurochemical mechanisms of opioid addiction are difficult due to the complexity of behavior and multiplicity of involved neurotransmitter and hormonal systems. The aim of this study was to examine the benefits of structured analysis of these mechanisms using the framework of the neurochemical model Functional Ensemble of Temperament (FET) and the example of maternal behavior under the condition of opium consumption in pregnancy. The FET differentiates between (a) endurance, (b) speed of integration, and (c) emotionality aspects of behavior suggesting that these systems are differentially regulated by (a) serotonin-neuropeptides-brain-derived neurotrophic factor (BDNF), (b) dopamine-GABA, and (c) opioid receptor systems, correspondingly. The FET also suggests that mu-opioid receptors (MORs) binding the endorphines (including opium’s ingredient morphine) have a stronger association with regulation endurance, whereas delta-OR have a stronger association with integration of behavior and kappa-OR – with the perceptual mobilization seen in anxiety. To test the predictions of this model, we compared the impact of massive MOR dysregulation on 3 behavioral aspects of behavior and on serotonin, BDNF, and corticosterone levels. <b><i>Methods:</i></b> The study used 24 female white Wistar rats which were randomly divided into (1) control group: pregnant rats without any intervention; (2) opium-exposed group: animals that were exposed to opium during pregnancy and after the delivery until the end of the study. At the end of the study, the levels of BDNF, serotonin (5-HT) in the hippocampus of the mother’s brain, and serum corticosterone, as well as 12 aspects of the maternal behavior were evaluated. The differences between control and experimental groups were assessed using the <i>t</i> test for independent samples. <b><i>Results:</i></b> The BDNF and serotonin concentrations in the hippocampus of the mother rats which were exposed to opium were lower than in the control group; the mean corticosterone in exposed mothers was higher than in the control group. Behaviorally, opium-consuming mothers showed lower endurance in 4 distinct behavioral categories (nesting, feeding, grooming, and retrieval) than the mothers in the control group. Ease of integration of behavior was affected to a lesser degree, showing a significant effect only in 1 out of 5 applied measures. Self-grooming, seen as an emotionality-related aspect of behavior, was not affected. <b><i>Conclusion:</i></b> Opium exposure during pregnancy in our experiment primarily reduced the endurance of rat’s maternal behavior, but the speed of integration of behavioral acts was less affected. This negative impact of opium on endurance was associated with a decrease of BDNF and serotonin levels in the hippocampus and an increase in corticosterone level in opium-consuming mothers. There is no effect of opium exposure on self-grooming behavior. This pattern supports the FET hypothesis about the role of 5-HT and BDNF in endurance, differential regulation of endurance, integrative and emotionality aspects of behavior, and differential association of the MOR system with endurance aspects, in comparison with kappa- and delta opioid receptors.
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Schiavone, Stefania, Margherita Neri, Angela Maffione, Paolo Frisoni, Maria Morgese, Luigia Trabace, and Emanuela Turillazzi. "Increased iNOS and Nitrosative Stress in Dopaminergic Neurons of MDMA-Exposed Rats." International Journal of Molecular Sciences 20, no. 5 (March 12, 2019): 1242. http://dx.doi.org/10.3390/ijms20051242.
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Several mechanisms underlying 3,4-Methylenedioxy-N-methylamphetamine (MDMA) neurotoxicity have been proposed, including neurochemical alterations and excitotoxicity mediated by reactive oxygen species (ROS), nitric oxide (NO), and reactive nitrogen species (RNS). However, ROS, NO, and RNS sources in the brain are not fully known. We aimed to investigate possible alterations in the expression of the ROS producer NOX enzymes (NOX2, NOX1, and NOX4), NO generators (iNOS, eNOS, and nNOS), markers of oxidative (8-hydroxy-2′-deoxyguanosine, 8OHdG), and nitrosative (3-nitrotyrosine, NT) stress, as well as the colocalization between cells positive for the dopamine transporter (DT1) and cells expressing the neuronal nuclei (NeuN) marker, in the frontal cortex of rats receiving saline or MDMA, sacrificed 6 h, 16 h, or 24 h after its administration. MDMA did not affect NOX2, NOX1, and NOX4 immunoreactivity, whereas iNOS expression was enhanced. The number of NT-positive cells was increased in MDMA-exposed animals, whereas no differences were detected in 8OHdG expression among experimental groups. MDMA and NT markers colocalized with DT1 positive cells. DT1 immunostaining was found in NeuN-positive stained cells. Virtually no colocalization was observed with microglia and astrocytes. Moreover, MDMA immunostaining was not found in NOX2-positive cells. Our results suggest that iNOS-derived nitrosative stress, but not NOX enzymes, may have a crucial role in the pathogenesis of MDMA-induced neurotoxicity, highlighting the specificity of different enzymatic systems in the development of neuropathological alterations induced by the abuse of this psychoactive compound.
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Samuel, D., O. Blin, N. Dusticier, and A. Nieoullon. "Effects of riluzole (2-amino-6-trifluoromethoxy benzothiazole) on striatal neurochemical markers in the rat, with special reference to the dopamine, choline, GABA and glutamate synaptosomal high affinity uptake systems." Fundamental & Clinical Pharmacology 6, no. 4-5 (June 1992): 177–84. http://dx.doi.org/10.1111/j.1472-8206.1992.tb00109.x.
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Spindler, Lennart R. B., Andrea I. Luppi, Ram M. Adapa, Michael M. Craig, Peter Coppola, Alexander R. D. Peattie, Anne E. Manktelow, et al. "Dopaminergic brainstem disconnection is common to pharmacological and pathological consciousness perturbation." Proceedings of the National Academy of Sciences 118, no. 30 (July 23, 2021): e2026289118. http://dx.doi.org/10.1073/pnas.2026289118.
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Clinical research into consciousness has long focused on cortical macroscopic networks and their disruption in pathological or pharmacological consciousness perturbation. Despite demonstrating diagnostic utility in disorders of consciousness (DoC) and monitoring anesthetic depth, these cortico-centric approaches have been unable to characterize which neurochemical systems may underpin consciousness alterations. Instead, preclinical experiments have long implicated the dopaminergic ventral tegmental area (VTA) in the brainstem. Despite dopaminergic agonist efficacy in DoC patients equally pointing to dopamine, the VTA has not been studied in human perturbed consciousness. To bridge this translational gap between preclinical subcortical and clinical cortico-centric perspectives, we assessed functional connectivity changes of a histologically characterized VTA using functional MRI recordings of pharmacologically (propofol sedation) and pathologically perturbed consciousness (DoC patients). Both cohorts demonstrated VTA disconnection from the precuneus and posterior cingulate (PCu/PCC), a main default mode network node widely implicated in consciousness. Strikingly, the stronger VTA–PCu/PCC connectivity was, the more the PCu/PCC functional connectome resembled its awake configuration, suggesting a possible neuromodulatory relationship. VTA-PCu/PCC connectivity increased toward healthy control levels only in DoC patients who behaviorally improved at follow-up assessment. To test whether VTA–PCu/PCC connectivity can be affected by a dopaminergic agonist, we demonstrated in a separate set of traumatic brain injury patients without DoC that methylphenidate significantly increased this connectivity. Together, our results characterize an in vivo dopaminergic connectivity deficit common to reversible and chronic consciousness perturbation. This noninvasive assessment of the dopaminergic system bridges preclinical and clinical work, associating dopaminergic VTA function with macroscopic network alterations, thereby elucidating a critical aspect of brainstem–cortical interplay for consciousness.
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Goldstein, LE, AM Rasmusson, BS Bunney, and RH Roth. "The NMDA glycine site antagonist (+)-HA-966 selectively regulates conditioned stress-induced metabolic activation of the mesoprefrontal cortical dopamine but not serotonin systems: a behavioral, neuroendocrine, and neurochemical study in the rat." Journal of Neuroscience 14, no. 8 (August 1, 1994): 4937–50. http://dx.doi.org/10.1523/jneurosci.14-08-04937.1994.
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Camporesi, Sara, Ines Khadimallah, Margot Fournier, Philippe Golay, Lijing Xin, Philipp S. Baumann, Martine Cleusix, et al. "M16. PROFILING GLUTAMATE AND D-SERINE PATHWAYS IN TREATMENT RESISTANT EARLY PSYCHOSIS PATIENTS." Schizophrenia Bulletin 46, Supplement_1 (April 2020): S139. http://dx.doi.org/10.1093/schbul/sbaa030.328.
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Abstract Background Pharmacological, neurochemical and electrophysiological studies provide compelling evidence that N-methyl-D-aspartate-receptor (NMDAR) hypofunction is a pathologic feature of schizophrenia (SZ). GWAS studies highlighted risk genes such as Serine Racemase (SRR), which synthesizes D-Serine (D-Ser), the co-agonist of glycine site at NMDARs, and Serine Hydroxymethyltransferase (SHMT1) which synthesizes L-Serine (L-Ser), the substrate of SRR. Around 30% of patients do not respond to dopamine modulation and are considered to suffer from treatment resistant SZ (TRS). While the exact cause of TRS remains unclear, multiple lines of evidence suggest the involvement of a dysregulation of the Glutamate (Glu) neurotransmission. To test the hypothesis whether Glu system dysregulation mediated by NMDAR hypofunction is an underlying mechanism of TRS, we investigate the Glu and D-Ser pathways in TRS and treatment responder (RESP) early psychosis patients (EPP). Methods From a total of 621 EPP aged 18 to 35, included in the TIPP (early Intervention Program in Lausanne, Baumann & al., 2013), 225 EPP were classified as TRS (n=33) or RESP (n=192) according to the strict Treatment Response and Resistance in Psychosis (TRRIP) criteria (Howes & al., 2017), with compliance ascertained by antipsychotic plasma levels. A matched healthy control (HC) group (N=114) was also recruited (DIGS criteria). No patient was taking clozapine at baseline. Clinical data was collected over a 3-year period. At baseline, following systems were assessed: 1) D-Ser pathway: plasmatic D-Ser, L-Ser and Glycine by HPLC (Hashimoto & al., 2016), protein levels of SRR and SHMT1 by ELISA; 2) Glu pathway: Glu and glutamine in plasma (HPLC) and prefrontal cortex (magnetic resonance spectroscopy, Xin & al., 2016). Results D-Ser pathway: in TRS, SRR levels were decreased by 56% as compared to RESP. Interestingly, we observed a positive correlation between plasma levels of D-Ser (SRR metabolite) and L-Ser (SRR substrate) in the TRS (r= 0.58; p =0.0015) but not in the RESP group, suggesting that SRR dysregulation might be a limiting factor in TRS patients. Moreover, in TRS patients, SHMT1 levels were decreased by 15% as compared to RESP, with a positive correlation between the substrate and metabolite of SHMT1, glycine and L-Ser (r =0.48; p =0.011). Dysregulation of SHMT1 might thus be a limiting factor in the TRS group. As compared to HC, L-Ser and D-Ser were significantly increased in patients (p <0.001 for L-Ser, p =0.0001 for D-Ser). However, no difference was observed in D-Ser, L-Ser and glycine in TRS as compared to RESP, although L-Ser tended to be higher in male TRS patients (p =0.06). Glu pathway: comparing TRS with RESP patients, plasma Glu levels were increased in the TRS group (p <0.0001), whereas they were higher in both patient groups compared to HC (p <0.0001). Interestingly, plasma and brain Glu levels showed a negative correlation in EPP, mostly driven by RESP (r = -0.42; p =0.035), a correlation which was absent in HC. Global Assessment of Functioning (GAF): at baseline, TRS and RESP displayed the same range of GAF. After a 3-year follow-up, TRS patients had poorer functioning as compared to RESP group (p <0.0001). Discussion Taken together, our results suggest that the TRS group, in which the levels of SRR and SHMT1 were lower and Glu plasma levels were higher, display a different regulation of the synthesis, degradation and/or accumulation of D-Ser and Glu as compared to the RESP group. However, replication in larger groups is needed. Moreover, our findings highlighted a dysregulation of D-Ser and Glu pathways in TRS patients in their early phase of psychosis. On the clinical side, our results confirm the significantly poorer functioning outcome in TRS patients.
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Simon, Maria J., Maria A. Zafra, and Amadeo Puerto. "Differential rewarding effects of electrical stimulation of the lateral hypothalamus and parabrachial complex: Functional characterization and the relevance of opioid systems and dopamine." Journal of Psychopharmacology 33, no. 12 (July 8, 2019): 1475–90. http://dx.doi.org/10.1177/0269881119855982.
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Background: Since the discovery of rewarding intracranial self-stimulation by Olds and Milner, extensive data have been published on the biological basis of reward. Although participation of the mesolimbic dopaminergic system is well documented, its precise role has not been fully elucidated, and some authors have proposed the involvement of other neural systems in processing specific aspects of reinforced behaviour. Aims and methods: We reviewed published data, including our own findings, on the rewarding effects induced by electrical stimulation of the lateral hypothalamus (LH) and of the external lateral parabrachial area (LPBe) – a brainstem region involved in processing the rewarding properties of natural and artificial substances – and compared its functional characteristics as observed in operant and non-operant behavioural procedures. Results: Brain circuits involved in the induction of preferences for stimuli associated with electrical stimulation of the LBPe appear to functionally and neurochemically differ from those activated by electrical stimulation of the LH. Interpretation: We discuss the possible involvement of the LPBe in processing emotional-affective aspects of the brain reward system.
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Ma, Mingxue, Yao Ni, Zirong Chi, Wanqing Meng, Haiyang Yu, Jiangdong Gong, Huanhuan Wei, Hong Han, Xinran Wang, and Wentao Xu. "Multiplexed neurochemical transmission emulated using a dual-excitatory synaptic transistor." npj 2D Materials and Applications 5, no. 1 (February 22, 2021). http://dx.doi.org/10.1038/s41699-021-00205-4.
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AbstractThe ability to emulate multiplexed neurochemical transmission is an important step toward mimicking complex brain activities. Glutamate and dopamine are neurotransmitters that regulate thinking and impulse signals independently or synergistically. However, emulation of such simultaneous neurotransmission is still challenging. Here we report design and fabrication of synaptic transistor that emulates multiplexed neurochemical transmission of glutamate and dopamine. The device can perform glutamate-induced long-term potentiation, dopamine-induced short-term potentiation, or co-release-induced depression under particular stimulus patterns. More importantly, a balanced ternary system that uses our ambipolar synaptic device backtrack input ‘true’, ‘false’ and ‘unknown’ logic signals; this process is more similar to the information processing in human brains than a traditional binary neural network. This work provides new insight for neuromorphic systems to establish new principles to reproduce the complexity of a mammalian central nervous system from simple basic units.
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Reynolds, Lauren M., and Cecilia Flores. "Mesocorticolimbic Dopamine Pathways Across Adolescence: Diversity in Development." Frontiers in Neural Circuits 15 (September 8, 2021). http://dx.doi.org/10.3389/fncir.2021.735625.
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Mesocorticolimbic dopamine circuity undergoes a protracted maturation during adolescent life. Stable adult levels of behavioral functioning in reward, motivational, and cognitive domains are established as these pathways are refined, however, their extended developmental window also leaves them vulnerable to perturbation by environmental factors. In this review, we highlight recent advances in understanding the mechanisms underlying dopamine pathway development in the adolescent brain, and how the environment influences these processes to establish or disrupt neurocircuit diversity. We further integrate these recent studies into the larger historical framework of anatomical and neurochemical changes occurring during adolescence in the mesocorticolimbic dopamine system. While dopamine neuron heterogeneity is increasingly appreciated at molecular, physiological, and anatomical levels, we suggest that a developmental facet may play a key role in establishing vulnerability or resilience to environmental stimuli and experience in distinct dopamine circuits, shifting the balance between healthy brain development and susceptibility to psychiatric disease.
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Almeida, Andre, Hamed Celaymanian, Natalie Seel, Boris Zak, and Hamid R. Noori. "Mathematical Modeling of the Neuronal Processes in Sugar Addiction." Nature Precedings, February 7, 2011. http://dx.doi.org/10.1038/npre.2011.5546.2.
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AbstractIt has already been demonstrated that the body responds to enhanced intake of sugar and is conducive to a natural form of addiction. There are substantial neurochemical changes in the brain (especially dopamine and acetylcholine systems) similar to other addictive drugs. A mathematical model comprised by a system of delayed leaky integrate-and-*re equations is established to simulate the eff*ects of sugar on a reward-circuitry. Simulations with Neuron suggest agreement with the neurobiological hypotheses of hyperactivity of neural systems due to binge sugar intake.
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Ranaldi, Robert. "Dopamine and reward seeking: the role of ventral tegmental area." Reviews in the Neurosciences, January 28, 2014. http://dx.doi.org/10.1515/revneuro-2014-0019.
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AbstractReward seeking is controlled by conditioned stimuli (CSs). There is a positive relation between mesocorticolimbic dopamine (DA) and the performance of learned reward-directed behavior. The mechanisms by which reward-, including drug-, associated stimuli come to acquire the capacity to activate the DA systems are not fully understood. In this review, we discuss the possible neurochemical mechanisms within the ventral tegmental area that may be involved in how CSs acquire the capacity to activate ventral tegmental area (VTA) DA neurons based on principles of long-term potentiation in the VTA and the role of mesocorticolimbic DA in reward-related learning. We propose that CSs function as such because they acquire the capacity to activate VTA DA neurons. Furthermore, CSs come to acquire this control of VTA DA cells when there is coincident
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Skandali, Nikolina, Joonas Majuri, Juho Joutsa, Kwangyeol Baek, Eveliina Arponen, Sarita Forsback, Valtteri Kaasinen, and Valerie Voon. "The neural substrates of risky rewards and losses in healthy volunteers and patient groups: a PET imaging study." Psychological Medicine, February 11, 2021, 1–9. http://dx.doi.org/10.1017/s0033291720005450.
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Abstract Background Risk is an essential trait of most daily decisions. Our behaviour when faced with risks involves evaluation of many factors including the outcome probabilities, the valence (gains or losses) and past experiences. Several psychiatric disorders belonging to distinct diagnostic categories, including pathological gambling and addiction, show pathological risk-taking and implicate abnormal dopaminergic, opioidergic and serotonergic neurotransmission. In this study, we adopted a transdiagnostic approach to delineate the neurochemical substrates of decision making under risk. Methods We recruited 39 participants, including 17 healthy controls, 15 patients with pathological gambling and seven binge eating disorder patients, who completed an anticipatory risk-taking task. Separately, participants underwent positron emission tomography (PET) imaging with three ligands, [18F]fluorodopa (FDOPA), [11C]MADAM and [11C]carfentanil to assess presynaptic dopamine synthesis capacity and serotonin transporter and mu-opioid receptor binding respectively. Results Risk-taking behaviour when faced with gains positively correlated with dorsal cingulate [11C]carfentanil binding and risk-taking to losses positively correlated with [11C]MADAM binding in the caudate and putamen across all subjects. Conclusions We show distinct neurochemical substrates underlying risk-taking with the dorsal cingulate cortex mu-opioid receptor binding associated with rewards and dorsal striatal serotonin transporter binding associated with losses. Risk-taking and goal-directed control appear to dissociate between dorsal and ventral fronto-striatal systems. Our findings thus highlight the potential role of pharmacological agents or neuromodulation on modifying valence-specific risk-taking biases.
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Hersey, Melinda, Amanda K. Bacon, Lydia G. Bailey, Mark A. Coggiano, Amy H. Newman, Lorenzo Leggio, and Gianluigi Tanda. "Psychostimulant Use Disorder, an Unmet Therapeutic Goal: Can Modafinil Narrow the Gap?" Frontiers in Neuroscience 15 (May 26, 2021). http://dx.doi.org/10.3389/fnins.2021.656475.
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The number of individuals affected by psychostimulant use disorder (PSUD) has increased rapidly over the last few decades resulting in economic, emotional, and physical burdens on our society. Further compounding this issue is the current lack of clinically approved medications to treat this disorder. The dopamine transporter (DAT) is a common target of psychostimulant actions related to their use and dependence, and the recent availability of atypical DAT inhibitors as a potential therapeutic option has garnered popularity in this research field. Modafinil (MOD), which is approved for clinical use for the treatment of narcolepsy and sleep disorders, blocks DAT just like commonly abused psychostimulants. However, preclinical and clinical studies have shown that it lacks the addictive properties (in both behavioral and neurochemical studies) associated with other abused DAT inhibitors. Clinical availability of MOD has facilitated its off-label use for several psychiatric disorders related to alteration of brain dopamine (DA) systems, including PSUD. In this review, we highlight clinical and preclinical research on MOD and its R-enantiomer, R-MOD, as potential medications for PSUD. Given the complexity of PSUD, we have also reported the effects of MOD on psychostimulant-induced appearance of several symptoms that could intensify the severity of the disease (i.e., sleep disorders and impairment of cognitive functions), besides the potential therapeutic effects of MOD on PSUD.
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Li, Shu-Chen, Guido Biele, Peter N. C. Mohr, and Hauke R. Heekeren. "Aging and Neuroeconomics: Insights from Research on Neuromodulation of Reward-based Decision Making." Analyse & Kritik 29, no. 1 (January 1, 2007). http://dx.doi.org/10.1515/auk-2007-0107.
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Abstract‘Neuroeconomics’ can be broadly defined as the research of how the brain interacts with the environment to make decisions that are functional given individual and contextual constraints. Deciphering such brain-environment transactions requires mechanistic understandings of the neurobiological processes that implement value-dependent decision making. To this end, a common empirical approach is to investigate neural mechanisms of reward-based decision making. Flexible updating of choices and associated expected outcomes in ways that are adaptive for a given task (or a given set of tasks) at hand relies on dynamic neurochemical tuning of the brain’s functional circuitries involved in the representation of tasks, goals and reward prediction. Empirical evidence as well as computational theories indicate that various neurotransmitter systems (e.g., dopamine, norepinephrine, and serotonin) play important roles in reward-based decision making. In light of the apparent aging-related decline in various aspects of the dopaminergic system as well as the effects of neuromodulation on reward-related processes, this article focuses selectively on the literature that highlights the triadic relations between dopaminergic modulation, reward-based decision making, and aging. Directions for future research on aging and neuroeconomoics are discussed.
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Bradberry, C. W. "Comparison of Acute and Chronic Neurochemical Effects of Cocaine and Cocaine Cues in Rhesus Monkeys and Rodents: Focus on Striatal and Cortical Dopamine Systems." Reviews in the Neurosciences 19, no. 2-3 (January 2008). http://dx.doi.org/10.1515/revneuro.2008.19.2-3.113.
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Iglesias, Amanda G., and Shelly B. Flagel. "The Paraventricular Thalamus as a Critical Node of Motivated Behavior via the Hypothalamic-Thalamic-Striatal Circuit." Frontiers in Integrative Neuroscience 15 (June 18, 2021). http://dx.doi.org/10.3389/fnint.2021.706713.
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In this review, we highlight evidence that supports a role for the paraventricular nucleus of the thalamus (PVT) in motivated behavior. We include a neuroanatomical and neurochemical overview, outlining what is known of the cellular makeup of the region and its most prominent afferent and efferent connections. We discuss how these connections and distinctions across the anterior-posterior axis correspond to the perceived function of the PVT. We then focus on the hypothalamic-thalamic-striatal circuit and the neuroanatomical and functional placement of the PVT within this circuit. In this regard, the PVT is ideally positioned to integrate information regarding internal states and the external environment and translate it into motivated actions. Based on data that has emerged in recent years, including that from our laboratory, we posit that orexinergic (OX) innervation from the lateral hypothalamus (LH) to the PVT encodes the incentive motivational value of reward cues and thereby alters the signaling of the glutamatergic neurons projecting from the PVT to the shell of the nucleus accumbens (NAcSh). The PVT-NAcSh pathway then modulates dopamine activity and resultant cue-motivated behaviors. As we and others apply novel tools and approaches to studying the PVT we will continue to refine the anatomical, cellular, and functional definitions currently ascribed to this nucleus and further elucidate its role in motivated behaviors.
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Cui, Xiaoying, John J. McGrath, Thomas H. J. Burne, and Darryl W. Eyles. "Vitamin D and schizophrenia: 20 years on." Molecular Psychiatry, January 26, 2021. http://dx.doi.org/10.1038/s41380-021-01025-0.
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AbstractMany epidemiological studies have highlighted the link between vitamin D deficiency and schizophrenia. In particular, two prominent studies report an association between neonatal vitamin D deficiency and an increased risk of schizophrenia. In parallel, much has been learnt about the role of vitamin D in the developing central nervous system over the last two decades. Studies in rodent models of developmental vitamin D (DVD)-deficiency describe how brain development is altered leading to a range of neurobiological and behavioral phenotypes of interest to schizophrenia. While glutamate and gamma aminobutyric acid (GABA) systems have been little investigated in these models, alterations in developing dopamine systems are frequently reported. There have been far more studies reporting patients with schizophrenia have an increased risk of vitamin D deficiency compared to well controls. Here we have conducted a systematic review and meta-analysis that basically confirms this association and extends this to first-episode psychosis. However, patients with schizophrenia also have poorer general health, poorer diets, are frequently less active and also have an increased risk of other medical conditions, all factors which reduce circulating vitamin D levels. Therefore, we would urge caution in any causal interpretation of this association. We also summarize the inconsistent results from existing vitamin D supplementation trials in patients with schizophrenia. In respect to animal models of adult vitamin D deficiency, such exposures produce subtle neurochemical alterations and effects on cognition but do not appear to produce behavioral phenotypes of relevance to schizophrenia. We conclude, the hypothesis that vitamin D deficiency during early life may increase the risk of schizophrenia remains plausible and warrants ongoing research.
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Liu, Pei-Pei, Chih-Chang Chao, and Ruey-Ming Liao. "Task-Dependent Effects of SKF83959 on Operant Behaviors Associated With Distinct Changes of CaMKII Signaling in Striatal Subareas." International Journal of Neuropsychopharmacology, May 28, 2021. http://dx.doi.org/10.1093/ijnp/pyab032.
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Abstract Background SKF83959, an atypical dopamine (DA) D1 receptor agonist, has been used to test the functions of DA-related receptor complexes in vitro, but little is known about its impact on conditioned behavior. The present study examined the effects of SKF83959 on operant behaviors and assayed the neurochemical mechanisms involved. Methods Male rats were trained and maintained on either a fixed-interval 30-second (FI30) schedule or a differential reinforcement of low-rate response 10-second (DRL10) schedule of reinforcement. After drug treatment tests, western blotting assayed the protein expressions of the calcium-/calmodulin-dependent protein kinase II (CaMKII) and the transcription factor cyclic AMP response element binding protein (CREB) in tissues collected from 4 selected DA-related areas. Results SKF83959 disrupted the performance of FI30 and DRL10 behaviors in a dose-dependent manner by reducing the total number of responses in varying magnitudes. Moreover, the distinct profiles of the behavior altered by the drug were manifested by analyzing qualitative and quantitative measures on both tasks. Western-blot results showed that phospho-CaMKII levels decreased in the nucleus accumbens and the dorsal striatum of the drug-treated FI30 and DRL10 subjects, respectively, compared with their vehicle controls. The phospho-CREB levels decreased in the nucleus accumbens and the hippocampus of drug-treated FI30 subjects but increased in the nucleus accumbens of drug-treated DRL10 subjects. Conclusions Our results provide important insight into the neuropsychopharmacology of SKF83959, indicating that the drug-altered operant behavior is task dependent and related to regional-dependent changes of CaMKII-CREB signaling in the mesocorticolimbic DA systems.