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Libros sobre el tema "Noradrenaline"

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Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 16 de abril de 2024

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1

J, Heal David y Marsden C. A, eds. The Pharmacology of noradrenaline in the central nervous system. Oxford [England]: Oxford University Press, 1990.

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2

1960-, Fuchs Stefan y Auer Max 1962-, eds. Biochemistry and histocytochemistry research developments. Hauppauge, N.Y: Nova Science, 2009.

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3

Singh, Lakhbir. Modulation of a 5-hydroxytryptamine-related behaviour by noradrenaline and gaba. Birmingham: University of Aston. Department of Pharmaceutical Sciences, 1985.

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4

Ward, Valerie Lynn. Oxygen-derived free radicals and the pathogenesis of catecholamine cardiomyopathy. [New Haven, Conn: s.n.], 1993.

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5

Fiziologicheskai͡a rolʹ autoadrenoret͡septorov. Moskva: "Nauka", 1991.

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6

A, Ordway Gregory, Schwartz Michael A y Frazer Alan, eds. Brain norepinephrine: Neurobiology and therapeutics. Cambridge: Cambridge University Press, 2007.

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7

Kirkup, Anthony Joseph. Modulation of membrane currents and mechanical activity by noradrenaline and other agents in vascular smooth muscle. Manchester: University of Manchester, 1995.

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8

Ichishima, Eiji. Unique enzymes of Aspergillus fungi used in Japanese bioindustries. Hauppauge, N.Y: Nova Science Publishers, 2011.

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9

Hentschel, Erwin. Occurence and function of biogenic amines (5-hydroxytryptamine, dopamine, noradrenaline, adrenaline and octopamine) in invertebrates: Bibliography = Vorkommen und Funktion biogener Amine (5-hydroxytryptamin, Dopamin, Noradrenalin, Adrenalin und Octopamin) bei wirbellosen Tieren : Bibliographie. Jena: Universitätsbibliothek, 1986.

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10

Hentschel, Erwin. Occurrence and function of biogenic amines (5-hydroxytryptamine, dopamine, noradrenaline, adrenaline and octopamine) in invertebrates: Bibliography = Vorkommen und Funktion biogener Amine (5-hydroxytryptamin, Dopamin, Noradrenalin, Adrenalin und Octopamin) bei wirbellosen Tieren : Bibliographie. Jena: Universitätsbibliothek, 1986.

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11

ed, Vanhoutte Paul M. y International Symposium [on Return Circulation and Norepinephrine] (3rd : 1990 : Cairo, Egypt), eds. Return circulation and norepinephrine: An update : proceedings of the 3rd International Symposium held in Cairo (Egypt) March 12-17th, 1990. Paris: J. Libbey Eurotext, 1991.

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12

M, Vanhoutte Paul, ed. Return circulation and norepinephrine--an update: Proceedings of the 3rd International Symposium held in Cairo (Egypt) March 12-17th, 1990. Paris: John Libbey Eurotext, 1991.

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13

Alfred Benzon Symposium (23rd 1985 Royal Danish Academy of Sciences and Letters). The sympathoadrenal system: Physiology and pathophysiology : proceedings of the Alfred Benzon Symposium 23 held at the premises of the Royal Danish Academy of Sciences and Letters, Copenhagen, 25-29 August 1985. Copenhagen: Munksgaard, 1986.

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14

International Symposium on Towards the Use of Noradrenergic Agonists for the Treatment of Pain (1992 Versailles, France). Towards the use of noradrenergic agonists for the treatment of pain: Proceedings of the International Symposium on Towards the Use of Noradrenergic Agonists for the Treatment of Pain, held in Versailles, France, 20-21 March 1992. Editado por Besson Jean-Marie R y Guilbaud G. Amsterdam: Excerpta Medica, 1992.

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15

Zorec, Robert y Nina Vardjan. Noradrenergic Signaling and Astroglia. Elsevier Science & Technology Books, 2017.

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16

Zorec, Robert y Nina Vardjan. Noradrenergic Signaling and Astroglia. Elsevier Science & Technology Books, 2017.

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17

(Editor), Ronald J. Bradley, Adron R. Harris (Editor), Peter Jenner (Editor) y John Smythies (Editor), eds. The Neuromodulators (International Review of Neurobiology) (International Review of Neurobiology). Academic Press, 2005.

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18

Brain norepinephrine: Neurobiology and therapeutics. Cambridge: Cambridge University Press, 2007.

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19

Schwartz, Michael A., Gregory A. Ordway y Alan Frazer. Brain Norepinephrine: Neurobiology and Therapeutics. University of Cambridge ESOL Examinations, 2012.

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20

Schwartz, Michael A., Gregory A. Ordway y Alan Frazer. Brain Norepinephrine: Neurobiology and Therapeutics. Cambridge University Press, 2007.

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21

Schwartz, Michael A., Gregory A. Ordway y Alan Frazer. Brain Norepinephrine: Neurobiology and Therapeutics. Cambridge University Press, 2007.

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22

Schwartz, Michael A., Gregory A. Ordway y Alan Frazer. Brain Norepinephrine: Neurobiology and Therapeutics. Cambridge University Press, 2007.

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23

Schwartz, Michael A., Gregory A. Ordway y Alan Frazer. Brain Norepinephrine: Neurobiology and Therapeutics. Cambridge University Press, 2009.

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24

Schwartz, Michael A., Gregory A. Ordway y Alan Frazer. Brain Norepinephrine: Neurobiology and Therapeutics. Cambridge University Press, 2007.

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25

James, Lee. Your Brain Electric: Everything you need to know about optimising neurotransmitters including serotonin, dopamine and noradrenaline. CreateSpace Independent Publishing Platform, 2014.

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26

Declerck, I. Modulation of the Ca2+ Movements in Vascular Smooth Muscle Cells by the Co-Transmitters Noradrenaline and ATP. Leuven University Press, 1991.

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27

Regional changes in brain noradrenergic activity following different types of exercise training in rats. 1990.

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28

Return Circulation and Norepinephrine. John Libbey & Co Ltd, 1991.

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29

Smythies, John R. The neuromodulators. vii, 285 p, 2005.

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30

(Editor), Ronald J. Bradley, Adron R. Harris (Editor), Peter Jenner (Editor) y John Smythies (Editor), eds. The Neuromodulators (International Review of Neurobiology) (International Review of Neurobiology). Academic Press, 2005.

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31

Regional changes in brain noradrenergic activity following different types of exercise training in rats. 1991.

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32

Regional changes in brain noradrenergic activity following different types of exercise training in rats. 1991.

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33

Hendrickson, Rebecca C. y Murray A. Raskind. Pharmacological Treatment of Nightmares, Sleep Disturbance, and Daytime Hyperarousal in PTSD: The Role of Prazosin, Other Noradrenergic Modulators, and Sedative Hypnotics or Commonly Used Sedating Medications. Editado por Charles B. Nemeroff y Charles R. Marmar. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190259440.003.0035.

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Disruption of stress-response systems contributes to the pathophysiology of post-traumatic stress disorder (PTSD). Consistent with this, daytime hyperarousal and nighttime sleep disruption, including trauma-related nightmares, are core symptoms of the disorder, often requiring targeted pharmacologic treatment. Although a variety of medications that target sleep–wake and arousal mechanisms are commonly used for this purpose, there remains the best empirical support for prazosin, a brain-active antagonist of the α‎1 noradrenaline receptor, with emerging evidence for doxazosin, a longer-acting medication with the same mechanism of action. This chapter reviews the evidence for use of prazosin and doxazosin as well as for the sedative hypnotics (benzodiazepines, nonbenzodiazepine hypnotics, and related medications), antihistamines, and sedating antidepressants trazodone and nefazodone to address hyperarousal symptoms and trauma-associated nightmares in PTSD. Clinical recommendations for the use of prazosin in PTSD, as well as a discussion of emerging pharmacologic treatments, are also included.
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34

Finnerup, Nanna Brix y Troels Staehelin Jensen. Management issues in neuropathic pain. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0133.

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Neuropathic pain is a common complication to cancer, cancer treatment, HIV, and other conditions that may affect the somatosensory nervous system. Neuropathic pain may be present in up to 40% of cancer patients and may persist independently of the cancer and affect the quality of life in disease-free cancer survivors. Particular surgical treatment and chemotherapy may cause chronic persistent neuropathic pain in cancer survivors. The diagnosis of neuropathic pain can be challenging and requires documentation of a nervous system lesion and pain in areas of sensory changes. The pharmacological treatment may include tricyclic antidepressants, selective serotonin noradrenaline reuptake inhibitors (duloxetine or venlafaxine), calcium channel α2↓ agonists (gabapentin or pregabalin), and opioids. Topical lidocaine and capsaicin, NMDA antagonists, carbamazepine, oxcarbazepine, and cannabinoids may be indicated. Due to limited efficacy or intolerable side effects at maximal doses, combination therapy is often required and careful monitoring of effect and adverse reactions is important.
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35

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

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Pharmacological influences on cognition and behaviour are often accompanied by effects on different aspects of attention. The actions of many psychoactive drugs (often used in the treatment of psychiatric disorders) depend on effects exerted on the classical chemical modulatory neurotransmitter systems including acetylcholine, and the monoamines, dopamine, noradrenaline and serotonin (or 5-hydroxytryptamine, 5-HT). These chemical systems originate in the reticular core of the brain and modulate attention by actions on forebrain structures including the thalamus, striatum, and the neocortex (especially the prefrontal cortex). Current research is attempting to dissect separable functions of these chemical neurotransmitters in mediating attention in relation to states of arousal and stress in comparable test paradigms in experimental animals and humans. New directions in research in this area are also identified, including the functions of the novel neurotransmitter orexin, and the role of GABA and glutamate in gamma oscillations and the network properties of the neocortex.
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36

Henriksen, Ole y Niels Juel Christensen. The Sympathoadrenal System: Physiology and Pathophysiology (Alfred Benzon Symposium, 23). Lippincott Williams & Wilkins, 1986.

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37

The Sympathoadrenal System. Munksgaard International Publishers, 1986.

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38

Jones, Barbara E. Neuroanatomical, neurochemical, and neurophysiological bases of waking and sleeping. Editado por Sudhansu Chokroverty, Luigi Ferini-Strambi y Christopher Kennard. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199682003.003.0004.

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Neurons distributed through the reticular core of the brainstem, hypothalamus, and basal forebrain and giving rise to ascending projections to the cortex or descending projections to the spinal cord promote the changes in cortical activity and behavior that underlie the sleep–wake cycle and three states of waking, NREM (slow wave) sleep, and REM (paradoxical) sleep. Forming the basic units of these systems, glutamate and GABA cell groups are heterogeneous in discharge profiles and projections, such that different subgroups can promote cortical activation (wake/REM(PS)-active) versus cortical deactivation (NREM(SWS)-active) by ascending influences or behavioral arousal with muscle tone (wake-active) versus behavioral quiescence with muscle atonia (NREM/REM(PS)-active) by descending influences. These different groups are in turn regulated by neuromodulatory systems, including cortical activation (wake/REM(PS)-active acetylcholine neurons), behavioral arousal (wake-active noradrenaline, histamine, serotonin, and orexin neurons), and behavioral quiescence (NREM/REM(PS)-active MCH neurons). By different projections, chemical neurotransmitters and discharge profiles, distinct cell groups thus act and interact to promote cyclic oscillations in cortical activity and behavior forming the sleep-wake cycle and states.
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