Relevant bibliographies by topics / Neurochemistry

Academic literature on the topic 'Neurochemistry'

Author: Grafiati
Published: 4 June 2021
Last updated: 29 July 2024

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Journal articles on the topic "Neurochemistry"

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Ramsey, R. B. "Neurochemistry." Transactions of the Zoological Society of London 33, no. 2 (July 8, 2010): 153–58. http://dx.doi.org/10.1111/j.1096-3642.1976.tb00048.x.

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Berezov, T. T. "Neurochemistry." Biochemical Education 25, no. 4 (October 1997): 249. http://dx.doi.org/10.1016/s0307-4412(97)87555-3.

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Benarroch, Eduardo E. "Neurochemistry." JAMA 295, no. 10 (March 8, 2006): 1190. http://dx.doi.org/10.1001/jama.295.10.1191-b.

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Stahl, S. M., S. D. Iversen, and E. C. Goodman. "Cognitive Neurochemistry." International Clinical Psychopharmacology 4, no. 4 (October 1989): 329–30. http://dx.doi.org/10.1097/00004850-198910000-00009.

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Williams, A. "Clinical Neurochemistry." Journal of Neurology, Neurosurgery & Psychiatry 51, no. 2 (February 1, 1988): 319–20. http://dx.doi.org/10.1136/jnnp.51.2.319.

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Koeppen, Arnulf H. "Basic Neurochemistry." Journal of the Neurological Sciences 174, no. 1 (March 2000): 49–50. http://dx.doi.org/10.1016/s0022-510x(00)00257-4.

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Holmes, Gregory L. "Basic neurochemistry." Journal of Epilepsy 7, no. 4 (January 1994): 337. http://dx.doi.org/10.1016/0896-6974(94)90102-3.

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Hashim, George A. "Clinical Neurochemistry." Neurochemistry International 11, no. 2 (January 1987): 248. http://dx.doi.org/10.1016/0197-0186(87)90018-0.

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Jean-Marie Matthieu, M. D. "Clinical neurochemistry." Neurochemistry International 11, no. 3 (January 1987): 351. http://dx.doi.org/10.1016/0197-0186(87)90057-x.

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Osborne, Neville. "Basic neurochemistry." Neurochemistry International 25, no. 2 (August 1994): 201. http://dx.doi.org/10.1016/0197-0186(94)90040-x.

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Dissertations / Theses on the topic "Neurochemistry"

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Pearson, Sally Jane. "The neurochemistry of Huntington's disease." Thesis, University of Nottingham, 1992. http://eprints.nottingham.ac.uk/28467/.

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This thesis describes the study of the neurochemistry of Huntington's disease using a large series of post mortem brain tissue taken from patients with Huntington's disease and from matching controls with no previous history of neuropsychiatric disorder. There were two main aims: firstly, to identify and characterise any altered parameters of neurotransmitter systems, especially in relation to the symptomatology of the disease; secondly, to understand the role of neurotoxins in the aetiology of the disease, particularly endogenous compounds that may have derived from aberrant metabolism. Concentrations of the amino acid transmitters, GABA and glutamate, were generally significantly decreased throughout the brain in Huntington's disease, including cortical and limbic regions. Cortical deficits were not associated with the dementia of the disease, whereas caudate levels of GABA and glutamate showed a relationship with the dementia. In patients with severe chorea, the medial pallidum was found to have a relatively smaller GABA deficit than mildly choreic patients. Another novel finding was that 5HT and 5HIAA concentrations were significantly increased in most regions of the brain in Huntington's disease, perhaps reflecting abnormal tryptophan metabolism. Such changes in the cortex provide evidence for a cortical involvement in the disease. Dopamine metabolism appeared to be reduced in Huntington's disease, reflected by the significantly decreased concentrations of its major metabolite, homovanillic acid, in most regions except for the cortex (where it was increased). Neuroactive compounds of the kynurenine pathway of tryptophan metabolism were measured in Huntington's disease. Quinolinic acid concentrations were not significantly altered, however 3- hydroxykynurenine concentrations were significantly increased in the striatum and cortex. This provides the first evidence for increased concentrations of an endogenous neurotoxic compound in the brain in Huntington's disease.
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Hadjihambi, Anna. "Neurochemistry of the hepatic encephalopathy." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10038691/.

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The pathogenesis of hepatic encephalopathy (HE) in cirrhosis is multifactorial and the role of ammonia remains controversial. Experimental studies conducted in animal (rat) models of HE, in combination with pharmacological approaches, were used to test the hypothesis that during HE, chronic exposure to elevated ammonia concentrations alters cerebral oxygenation, compromises lactate transport between astrocytes and neurons, and impairs uptake of neurotransmitters. It was also hypothesised that HE impairs glymphatic clearance mechanisms, either as a cause or a consequence of the disease, which exacerbates the detrimental central nervous effects of the accumulated toxins. The results of the experiments described in this thesis suggest that in HE: a) ammonia compromises cerebral oxygenation, but does not affect cerebrovascular reactivity, b) ammonia mediates cortical hemichannel dysfunction and impairs channel-mediated lactate release, potentially interfering with the astrocyte-neuron lactate shuttle, c) hyperammonemia results in a significant increase in cortical extracellular glutamate concentration, which is exacerbated under hypoxic conditions, and d) efficacy of glymphatic clearance is affected in discrete regions of the brain, which aligns with specific cognitive/behavioral impairments. These findings provide the first evidence of a critical pathophysiological role of ammonia in inducing neuronal energy deficit in HE due to impaired cerebral oxygenation, compromised hemichannel-mediated lactate transport between astrocytes and neurons and affected glymphatic clearance.
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Myint, Aye Mu. "Neurochemistry immune systems interaction in depressions." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Universiteit Maastricht [host], 2007. http://arno.unimaas.nl/show.cgi?fid=6834.

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Warren, Naomi M. "The cholinergic neurochemistry of progressive supranuclear palsy." Thesis, University of Newcastle upon Tyne, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.432505.

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McAfee, Ghia. "Smoking and brain dopaminergic neurochemistry / Ghia McAfee." Thesis, North-West University, 2004. http://hdl.handle.net/10394/590.

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Tobacco use is not only a major health concern worldwide but also a grotesque economic burden on the smoker as well as the health care system. The most well-known and most researched constituent of tobacco products is nicotine. There are a variety of products on the market that ensure nicotine intake, including cigarettes, cigars, pipe tobacco and smokeless tobacco. Once absorbed by the body, nicotine undergoes phase I metabolism by cytochrome P450 (CYP) 2A6 (humans) or CYP2B1 (rat) to cotinine, the major metabolite. Since nicotine is a blood flow marker, its transport across the blood-brain barrier (BBB) has been well documented. However, data on the BBB penetration of nicotine and cotinine in animals subject to chronic nicotine exposure are limited. This gap in literature was identified and subsequently the focus of our first objective. Our data indicate that neither nicotine or cotinine uptake by the BBB is altered after chronic nicotine exposure in rat. Nicotine exerts its effect by binding to nicotinic cholinergic receptors (nAChRs) on dopaminergic neurons in the striatum and the ventral tegmental area (VTA). The addictive property of nicotine is attributed to its effects on the mesocorticolimbic system, which serves a fundamental role in the acquisition of behaviours. Smoking not only plays a role in addiction but also in Parkinson's disease (PD), where epidemiological studies have shown that smokers have a lower incidence of PD as opposed to non-smokers. Dopamine (DA) is one of the major neurotransmitters that plays a critical role in addiction and PD. Centrally, the biosynthesis of DA occurs intraneuronally through the ratelimiting enzyme, tyrosine hydroxylase (TH). DA undergoes metabolism by monoamine oxidase (MAO) intraneuronally. DA, that is not metabolized by MAO, is subsequently transported into the storage vesicles. After stimulation of nAChRs, DA is released into the synaptic cleft after membrane depolarization. Released DA stimulates post-synaptic dopaminergic receptors, is metabolized by catecholamine-0-methyl-transferase or transporter back into the pre-synaptic neuron by DA transporter (DAT). Little is known about the effects of whole cigarette smoke on the dopaminergic system. Therefore, our second objective of this study was to determine the effect of whole cigarette smoke extract (nicotine-containing and nicotine-free smoke extract), nicotine and cotinine on TH and DAT expression in undifferentiated pheochromocytoma cells. Our third objective was closely developed from our second. After investigating the effect in vitro, we determined the effect in vivo in rats after 28 day exposure of whole cigarette smoke extract (nicotine-containing and nicotine-free smoke extract), nicotine and cotinine on TH and DAT regulation. Both the in vitro and in vivo TH as well as the in vivo DAT regulation data implicated nicotine to be responsible for TH and DAT upregulation. It is known that nicotine releases DA from rat striatal synaptosomes. We therefore aimed to determine whether a component of tobacco leaf extracts which is a MAO-A and MAO-B inhibitor, 2,3,6-trimethyl-I,4-naphthoquinone (TMN) release DA from rat striatal synaptosomes. We found that TMN releases DA from synaptosomes, to a greater extent when compared to nicotine. Our data conclude that cotinine does cross the BBB and that both nicotine and cotinine transport do not vary after chronic nicotine exposure. We also found that nicotine, as the major constituent of tobacco smoke, is responsible for increased DA synthesis and DA transport back into the presynaptic neuron. TMN, is not only a MAO-A and MAO-B inhibitor but experiments from our laboratory indicate that in striatal synaptosomes, TMN releases DA to a greater extent than nicotine.
Thesis (Ph.D. (Pharmaceutical Chemistry))--North-West University, Potchefstroom Campus, 2005.
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Ghazaleh, Haya Abu. "The neurochemistry of rat imidazoline binding sites." Thesis, University of Bristol, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.442183.

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Aguilar, Carolina. "Pesticides and pesticide combinations on brain neurochemistry." Thesis, Virginia Tech, 2004. http://hdl.handle.net/10919/34697.

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Pesticides have been suggested to play a role in the development of many neurodegerative diseases including Parkinson's disease and Alzheimer's disease. Additionally, it has been suggested that exposure to pesticides and other environmental chemicals during the early stages of life could result in an increased vulnerability to such substances that could lead to neurotoxicity and degeneration late in life. We hypothesized that exposure to mixtures of certain pesticides could change neurotransmitter levels and cellular oxidative stress and that this would be greater in mice exposed early and later in life than mice exposed only as adults. We studied the effects of permethrin (PR) (a pyrethroid type I) and endosulfan (EN) (an organochlorine) on the levels of catecholamines, indolamines, acetylcholinesterase, lipid peroxidation and α-synuclein in the brain of mice. These pesticides have different structures but both are known to modify the kinetics of voltage-sensitive ion channels and calcium ion flux/homeostasis that could affect the release of several neurotransmitters. The study consisted of two experiments: In the first experiment, adult C57Bl/6 mice (7-9 months old) were injected, intraperitoneally, with the following treatments: EN 4.3, 2.15 mg/kg; PR 150, 15 mg/kg and their mixtures EN 4.3 + PR 150 and EN 2.15 + PR 15 mg/kg. Mice were sacrificed 24 hrs after the last injection. In the second experiment, doses consisted of EN 0.7, 1.4 mg/kg, PR 1.5, 15 mg/kg and their mixtures EN 0.7 + PR 1.5 mg/kg and EN 1.4 + PR 15 mg/kg were given to juvenile mice intraperitoneally daily during a period of two weeks from postnatal day 5 to 19. Mice were then, left undisturbed with their dams. Re-challenge was performed when mice were 7-9 months old and dosages of EN 4.3, 2.15 mg/kg, PR 150, 15 mg/kg and their mixtures, EN 4.3 + PR 150 and EN 2.15 + PR 15 mg/kg were given intraperitoneally every other day during a period of two weeks to match the treatments when pesticide exposure was only as adults. Mice were sacrificed 24 hrs after the last injection.

The corpora striatum was extracted and analyzed by HPLC for catecholamines (dopamine, DOPAC, homovalinic acid and norepinephrine) and indolamines (serotonin and 5-HIAA). In general low doses of permethrin and endosulfan alone and in combination (EN 2.15 + PR 15 mg/kg) altered the levels of catecholamines and indolamines in both studies with adult mice and mice dosed as juveniles and re-challenged as adults. Catecholamine and indolamines levels were affected to a greater extent in the adult mice than in mice dosed as juveniles and re-challenged as adults, when compared to controls.

Acetylcholinesterase was increased under both exposure situations but again adult mice seemed to be more affected than mice dosed as juveniles and re-challenged as adults.

Because reactive oxygen species have been implicated in the development of Parkinson's disease, and are known to cause degradation of certain neurotransmitters, we monitored the levels of lipid peroxides in brain cortex as an indicator of free radical tissue damage. The peroxide levels were measured by thiobarbituric acid reactive products (TBARS). Increased levels of lipid peroxides were significant in the low dose treatment groups of the adult study. However, there seemed to be a pattern between the levels of dopamine and DOPAC in the striatum and the levels of peroxidation in cortex. The presence of dopamine metabolites appeared to be related to high levels of peroxidation within the basal ganglia and up-regulation of proteins such as α-synuclein. Western blots of α-synuclein in both experiments of the study showed intense double and triple bands that corresponded to aggregated α-synuclein. In general, when compared with controls, mice dosed as juveniles and re-challenged as adults did not alter the above parameters as much as mice dosed only as adults. Instead, the mice first dosed as juveniles seemed to develop an adaptation response to the later exposure of these pesticides.

Taking all these results into account, early exposure and re-challenge with permethrin and endosulfan in this study appeared to induce a protective response against neurochemical changes in the brain of these mice. In addition, low doses of these pesticides and the low dose combination mixture seem to exert an effect on the parameters studied.

Therefore, exposure to pesticides such as endosulfan and permethrin and their combinations could make a contribution towards the initiation or aggravation of biochemical neurodegenerative diseases such as Parkinson's and Alzheimer's diseases.


Master of Science
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Furnish, Oehrtman Elizabeth Jean. "The role of gelsolin upregulation and overexpression in neurite outgrowth for PC12 cells." Access restricted to users with UT Austin EID Full text (PDF) from UMI/Dissertation Abstracts International, 2001. http://wwwlib.umi.com/cr/utexas/fullcit?p3031599.

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Durieux, Alice Marie Sybille. "Neurochemistry in autism spectrum disorder : a translational approach." Thesis, King's College London (University of London), 2017. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.718590.

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The pathogenesis of autism spectrum disorder (ASD) may include dysfunction of brain Redox homeostasis and abnormalities in the balance between neuronal excitation (E) and inhibition (I). Both systems have therefore been put forward as potential treatment targets for the development of new pharmacotherapies for the condition. However, ASD is a highly heterogeneous disorder, and it is unclear whether altered oxidative metabolism and/or E/I imbalance occur in all individuals with ASD. Therefore in the first part of this thesis (Study 1), I examined markers of Redox metabolism in a cohort of adult males with ASD already known to have E/I anomalies. Next, I undertook a series of preclinical studies (Studies 2- 4) to investigate whether pharmacological modulation of Redox and/or E/I alters neurochemistry and behaviour in mouse models of ASD. I used in vivo proton magnetic resonance spectroscopy ([1H]MRS) to quantify glutathione (GSH - the major endogenous antioxidant), as a marker of Redox metabolism; and glutamate and GABA (respectively the major excitatory and inhibitory neurotransmitters), as markers of E/I balance. In Study 1, I found GSH was unaltered in adult males with ASD already known to have glutamatergic anomalies. Therefore, my preclinical work focussed upon the regulation of E/I balance. Because the role of glia in E/I and ASD is under-explored, I examined modulation of glutamate by glial mechanisms. In Study 2, I provided proof-of-concept evidence that N-Acetylcysteine (NAC), a compound that activates the cystine-glutamate antiporter of glial cells, reduces glutamate in wild-type C57BL/6J mice. I then sought to translate this finding to a mouse model of ASD with baseline E/I imbalance. After finding that mice lacking synaptic protein Neurexin 1α, a genetic model of ASD, have normal levels of striatal glutamate (Study 3), I excluded this model and instead administered NAC to BTBR mice, an inbred strain with a behavioural phenotype reminiscent of ASD (Study 4). I found that BTBR mice have a baseline E/I imbalance in the striatum and the prefrontal cortex, two brain regions involved in the core symptoms of ASD. These anomalies were partially normalised by NAC treatment, which also improved social interactions and repetitive digging, two behaviours relevant to the core symptoms of ASD. My results suggest that the glial regulatory mechanisms of E/I balance can be modulated pharmacologically, and have consequences for behaviours relevant to ASD. While my preclinical results suggest that the clinical utility of NAC in ASD deserves further exploration, the broader implications of my work are that glial cells are a potential target for the development of new treatments for ASD.
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Berners, Manfred Otto Maria. "Development of enzyme based sensors for use in neurochemistry." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307034.

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Books on the topic "Neurochemistry"

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Teelken, Albert, and Jaap Korf, eds. Neurochemistry. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9.

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Lajtha, Abel, ed. Pathological Neurochemistry. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4757-0797-7.

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M, Stahl S., Iversen Susan D. 1940-, Goodman E. C, and Neuroscience Research Centre (Merck Sharp & Dohme). Clinical Neuroscience Research Unit., eds. Cognitive neurochemistry. Oxford: Oxford University Press, 1987.

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1945-, Wiggins Richard C., McCandless David W. 1941-, and Enna S. J, eds. Developmental neurochemistry. Austin: University of Texas Press, 1985.

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G, Lunt George, and Olsen Richard W, eds. Comparative invertebrate neurochemistry. London: Croom Helm, 1988.

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Lunt, G. G., and R. W. Olsen, eds. Comparative Invertebrate Neurochemistry. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4615-9804-6.

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Mathew, Bijo, and Della Grace Thomas Parambi, eds. Principles of Neurochemistry. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-5167-3.

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Perry, Elaine K., Heather Ashton, and Allan H. Young, eds. Neurochemistry of Consciousness. Amsterdam: John Benjamins Publishing Company, 2002. http://dx.doi.org/10.1075/aicr.36.

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Oliver, Dolly J., ed. Neurotoxins in neurochemistry. Chichester: E. Horwood, 1988.

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Oliver, Dolly J., ed. Neurotoxins in neurochemistry. Chichester: E Horwood, 1988.

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Book chapters on the topic "Neurochemistry"

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Scott, Bonnie M., Sable Thompson, and Dawn Bowers. "Neurochemistry." In Encyclopedia of Gerontology and Population Aging, 1–7. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_672-1.

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Hoffmann, Michael. "Neurochemistry." In Cognitive, Conative and Behavioral Neurology, 35–49. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-33181-2_3.

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Anagnostou, Evdokia, Deepali Mankad, Joshua Diehl, Catherine Lord, Sarah Butler, Andrea McDuffie, Lisa Shull, et al. "Neurochemistry." In Encyclopedia of Autism Spectrum Disorders, 2014–15. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_1536.

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Scott, Bonnie M., Sable Thompson, and Dawn Bowers. "Neurochemistry." In Encyclopedia of Gerontology and Population Aging, 3424–30. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_672.

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Anderson, George M. "Neurochemistry." In Encyclopedia of Autism Spectrum Disorders, 3132–33. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-319-91280-6_1536.

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Huxtable, Ryan J., and Flavia Franconi. "Introduction: Neurochemistry." In Advances in Experimental Medicine and Biology, 247–52. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4899-0405-8_26.

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Bachelard, Herman. "A Brief History of the European Society for Neurochemistry." In Neurochemistry, 1–7. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_1.

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Long, S. K., and A. I. Bosch. "A Pharmacological Characterization Of Hippocampal 5-HT1D Receptors In The Guinea Pig." In Neurochemistry, 59–62. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_10.

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Reiter, Russel J. "Pharmacology of Melatonin as a Neural Antioxid Ant." In Neurochemistry, 599–603. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_100.

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Nowak, Jerzy Z., Jolanta B. Zawilska, Jolanta Rosiak, and Tomasz Kalaony. "Melatonin Biosynthesis in the Retina." In Neurochemistry, 605–9. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5405-9_101.

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Conference papers on the topic "Neurochemistry"

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Bozorgzadeh, Bardia, and Pedram Mohseni. "Integrated systems for high-fidelity sensing and manipulation of brain neurochemistry." In 2016 IEEE International Symposium on Circuits and Systems (ISCAS). IEEE, 2016. http://dx.doi.org/10.1109/iscas.2016.7538926.

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El Ansary, Maged, Nima Soltani, Hossein Kassiri, Ruben Machado, Suzie Dufou, Peter L. Carlen, Michael Thompson, and Roman Genov. "50nW 5kHz-BW opamp-less ΔΣ impedance analyzer for brain neurochemistry monitoring." In 2018 IEEE International Solid-State Circuits Conference (ISSCC). IEEE, 2018. http://dx.doi.org/10.1109/isscc.2018.8310297.

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"Pharmacological effects of arecoline on zebrafish behavior, neurochemistry, neurophysiology and brain gene expression." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-170.

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Smith, Adam R. "Comparing brain development and neurochemistry in social and solitary individuals of the sweat bee Megalopta genalis." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.114873.

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Ip, I. Betina, Claudia Lunghi, Uzay E. Emir, Andrew J. Parker, and Holly Bridge. "Relating Eye Dominance to Neurochemistry in the Human Visual Cortex Using Ultra High Field 7-Tesla MR Spectroscopy." In 2019 International Conference on 3D Immersion (IC3D). IEEE, 2019. http://dx.doi.org/10.1109/ic3d48390.2019.8976001.

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Sarkisova, Karine, Ekaterina Fedosova, Alla Shatskova, Victor Narkevich, and Vladimir Kudrin. "THE EFFECTS OF MATERNAL METHYL-ENRICHED DIET ON GENETIC ABSENCE EPILEPSY, COMORBID DEPRESSION AND THE BRAIN NEUROCHEMISTRY IN ADULT OFFSPRING OF WAG/RIJ RATS." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2311.sudak.ns2021-17/334-335.

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Reports on the topic "Neurochemistry"

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Yorio, Thomas. Vision Integrating Strategies in Ophthalmology and Neurochemistry (VISION). Fort Belvoir, VA: Defense Technical Information Center, February 2012. http://dx.doi.org/10.21236/ada606200.

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Yorio, Thomas. Vision Integrating Strategies in Ophthalmology and Neurochemistry (VISION). Fort Belvoir, VA: Defense Technical Information Center, February 2011. http://dx.doi.org/10.21236/ada606303.

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Clark, Abbot, and Thomas Yorio. Vision Integrating Strategies in Ophthalmology and Neurochemistry (VISION). Fort Belvoir, VA: Defense Technical Information Center, February 2014. http://dx.doi.org/10.21236/ada621384.

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Ernst, Thomas. Brain Function, Structure, and Neurochemistry After Tamoxifen/Chemotherapy Assessed by Neuropsychologic Testing and 1H Magnetic Resonance Spectroscopy. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada403373.

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Chlebowski, Rowan. Brain Function, Structure, and Neurochemistry After Tamoxifen/Chemotherapy Assessed by Neuropsychologic Testing and H Magnetic Resonance Spectroscopy. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412888.

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Glass, David J. Study of SCN Neurochemistry Using in Vivo Microdialysis in the Conscious Brain: Correlation with Overt Circadian Rhythms. Fort Belvoir, VA: Defense Technical Information Center, October 1991. http://dx.doi.org/10.21236/ada247172.

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Killgore, William. Effects of Bright Light Therapy of Sleep, Cognition, Brain Function, and Neurochemistry in Mild Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, January 2012. http://dx.doi.org/10.21236/ada562581.

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Killgore, William D., and Lily Preer. Effects of Bright Light Therapy on Sleep, Cognition, Brain Function, and Neurochemistry in Mild Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, January 2013. http://dx.doi.org/10.21236/ada583289.

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Killgore, William D., and Olga Tkachenko. Effects of Bright Light Therapy on Sleep, Cognition, Brain Function, and Neurochemistry in Mild Traumatic Brain Injury. Fort Belvoir, VA: Defense Technical Information Center, January 2014. http://dx.doi.org/10.21236/ada621257.

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