Relevant bibliographies by topics / Neurochemical dopamine systems

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Academic literature on the topic 'Neurochemical dopamine systems'

Author: Grafiati
Published: 4 June 2021
Last updated: 9 February 2022

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Journal articles on the topic "Neurochemical dopamine systems"

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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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Dissertations / Theses on the topic "Neurochemical dopamine systems"

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Last, A. T. J. "An electrophysiological study of neurochemical interactions in the substantia nigra." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382628.

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Floresco, Stanley Bogdan. "Limbic-striatal interactions and their modulation by dopamine : electrophysiological, neurochemical and behavioral analyses." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ48635.pdf.

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Bozorgzadeh, Bardia. "Integrated Microsystems for High-Fidelity Sensing and Manipulation of Brain Neurochemistry." Case Western Reserve University School of Graduate Studies / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=case1432223568.

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Abbott, Brendan. "Effort-Related Motivational Dysfunctions: Behavioral and Neurochemical Studies of the Wistar-Kyoto Rat Model of Depression." 2018. https://scholarworks.umass.edu/masters_theses_2/625.

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Depression and related disorders are characterized by motivational dysfunctions, including deficits in behavioral activation and exertion of effort. Animal models of relevance to depression represent a critical starting point in elucidating the neurobiological mechanisms underlying motivational dysfunctions. The present study explored the use of the Wistar-Kyoto (WKY) animal model of depression to examine effort-related functions as measured by voluntary wheel running and performance on a mixed fixed ratio 5/progressive ratio (FR5/PR) operant task. Given the known link between activational aspects of motivation and the mesocorticolimbic dopamine (DA) system, the behavioral effects of d-amphetamine (0.5 and 1.0 mg/kg, IP), a psychostimulant that increases DA release, were evaluated in WKY and control Sprague-Dawley (SD) male and female rats responding on a mixed FR5/PR task. An additional experiment assessed intracellular content of monoamine neurotransmitters and their metabolites in relevant mesocorticolimbic brain regions, including the medial prefrontal cortex, the nucleus accumbens and the ventrolateral striatum using HPLC-ED. WKY rats demonstrated initial effort-related deficits in FR5/PR responding compared to SD controls, which ameliorated with training. Amphetamine significantly decreased FR5 work output, but increased responding on the PR phase in both SD and WKY rats. This effect was more pronounced in SD rats compare to WKY rats. In addition, sex differences were evident both in FR5/PR performance and in the behavioral response to amphetamine treatment. Moreover, females demonstrated higher levels of voluntary wheel-running than males. Finally, tissue concentrations of dopamine were lower in the NA and VLS of WKY compared to SD rats. Taken together, results suggest dysfunctions in mesolimbic DA neurotransmission in the WKY strain, likely underlying the depressive phenotype. The present study represents an important initial step in validating the WKY strain as a rat model of effort-related dysfunctions relevant to depression and other neuropsychiatric disorders.
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Books on the topic "Neurochemical dopamine systems"

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

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

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Reynolds, G. P. "Amygdala Dopamine Asymmetry in Schizophrenia: Neurochemical Evidence for a Left Temporal Lobe Dysfunction." In Dopaminergic Systems and their Regulation, 285–91. London: Palgrave Macmillan UK, 1986. http://dx.doi.org/10.1007/978-1-349-07431-0_19.

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Robbins, Trevor W., and Barry J. Everitt. "Substance use disorders and the mechanisms of drug addiction." In New Oxford Textbook of Psychiatry, edited by John R. Geddes, Nancy C. Andreasen, and Guy M. Goodwin, 477–91. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198713005.003.0048.

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The understanding of drug addiction has gained much from a neuroscientific approach, reflected by changing approaches in diagnosis. The two main psychological accounts of addiction to substances, ranging from alcohol and nicotine to opioids and stimulant drugs, are opponent motivational processing, emphasizing the importance of withdrawal symptoms, and aberrant learning from positive reinforcement. The neural and neurochemical systems implicated have been identified on the basis of animal studies, using especially the self-administration paradigm, and human investigations employing a range of brain imaging modalities. These neural substrates include dopamine-dependent functions of the ventral and dorsal striatum, as well as regulatory influences of fronto-limbic systems. The chapter considers the critical issue of cause and effect, and whether brain changes reflect neurotoxic effects of abuse or whether there are predisposing neurobehavioural factors. It also outlines the current situation and future prospects for treatment by medication, possibly in association with psychological approaches.
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Wallace, Daniel J., and Janice Brock Wallace. "What is the Autonomic Nervous System?" In All About Fibromyalgia. Oxford University Press, 2002. http://dx.doi.org/10.1093/oso/9780195147537.003.0013.

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The autonomic nervous system (ANS) has already been introduced; let’s summarize what we know about it so far. Part of the peripheral nervous system, the ANS consists of the sympathetic nervous system (SNS), which consists of outflow from the thoracic and upper lumbar spine, and the parasympathetic nervous system (PNS), including outflow from the cranial nerves emanating from the upper spine and also from the mid-lumbar to the sacral areas at the buttock region. Several neurochemicals help transmit autonomic instructions. These include epinephrine (adrenaline), norepinephrine (noradrenalin), dopamine, and acetylcholine. This chapter will focus on how abnormalities in the regulation of the ANS cause many of the symptoms and signs observed in fibromyalgia. Our body has numerous receptors or surveillance sensors that detect heat, cold, and inflammation. These ANS sensors perform a function known as autoregulation. As an example of how the ANS normally works, why don’t we pass out when we suddenly jump out of bed? Because the ANS instantly constricts our blood vessels peripherally and dilates them centrally. In other words, as blood is pooled to the heart and the brain, the ANS adjusts our blood pressure and regulates our pulse, or heart rate, so that we don’t collapse. On the local level, these sensors dilate or constrict flow from blood vessels. They can secondarily contract and relax muscles, open and close lung airways, or cause us to sweat. For instance, ANS sensors can tone muscles, regulate urine, and regulate bowel movements, as well as dilate or constrict our pupils. The SNS arm of the ANS is our “fight or flight” system, releasing epinephrine and norepinephrine as well as a neurochemical called dopamine. Whereas the SNS often acts as an acute stress response, the PNS arm tends to protect and conserve body processes and resources. The SNS and PNS sometimes work at cross purposes, but frequently they work together to permit actions such as normal sexual functioning and urination. How do the workings of the ANS relate to fibromyalgia? The SNS is underactive in fibromyalgia in the sense that an increased ratio of excitatory to inhibitory responses from central sensitization results in lower blood flow rates, leaky capillaries, at relatively low baseline blood pressure.
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Mathias, Christopher J., and David A. Low. "Diseases of the autonomic nervous system." In Oxford Textbook of Medicine, edited by Christopher Kennard, 6150–65. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198746690.003.0603.

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The autonomic nervous system innervates all organs, producing predominantly involuntary and automatic actions that are mediated by two principal efferent pathways, the sympathetic and parasympathetic, which are neurochemically and anatomically distinct. Numerous synaptic relays and neurotransmitters allow the autonomic control of organ function at local and central levels to be integrated with the requirements of the whole body. The peripheral and central components of the autonomic nervous system are frequently affected by diseases, conditions, or toxins. Autonomic disorders are described as (1) primary—without defined cause, including multiple system atrophy and acute/subacute dysautonomias; or (2) secondary—with specific defects or as a consequence of other conditions, including diabetes mellitus, Riley–Day syndrome, amyloid neuropathy, dopamine β‎-hydroxylase deficiency, spinal cord injury, and many drugs.
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Amalric, Marianne, and George F. Koob. "Chapter 14 Functionally selective neurochemical afferents and efferents of the mesocorticolimbic and nigrostriatal dopamine system." In Progress in Brain Research, 209–26. Elsevier, 1993. http://dx.doi.org/10.1016/s0079-6123(08)61348-5.

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