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Libros sobre el tema "Dopaminergic neurons"

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Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 7 de julio de 2024

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1

Umberto, Di Porzio, Pernas-Alonso Roberto y Perrone-Capano Carla, eds. Development of dopaminergic neurons. Austin: R.G. Landes Co., 1999.

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2

Beart, P. M., G. N. Woodruff y D. M. Jackson, eds. Pharmacology and Functional Regulation of Dopaminergic Neurons. London: Palgrave Macmillan UK, 1988. http://dx.doi.org/10.1007/978-1-349-10047-7.

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3

Jeroen, Pasterkamp R., Smidt Marten P y Burbach, Johannes Peter Henri, 1954-, eds. Development and engineering of dopamine neurons. New York, N.Y: Springer Science+Business Media, 2009.

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4

Giovanni, Giuseppe. Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Vienna: Springer-Verlag Vienna, 2009.

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5

Giovanni, Giuseppe, Vincenzo Di Matteo y Ennio Esposito, eds. Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Vienna: Springer Vienna, 2009. http://dx.doi.org/10.1007/978-3-211-92660-4.

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6

Kjell, Fuxe y Wenner-Grenska samfundet, eds. Trophic regulation of the basal ganglia: Focus on dopamine neurons. Oxford, OX, UK: Pergamon, 1994.

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7

M, Beart P., Woodruff G. N, Jackson D. M y International Congress of Pharmacology, (10th : 1987 : Sydney, N.S.W.), eds. Pharmacology and functional regulation of dopaminergic neurons: Proceedings of a satellite symposium of the IUPHAR 10th International Congress of pharmacology, 31 Aug.- 2 Sep. 1987. Basingstoke: Macmillan, 1988.

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8

M, Beart P., Woodruff Geoffrey N, Jackson D. M, International Union of Pharmacology y International Congress of Pharmacology (10th : 1987 : Cessnock, N.S.W.).)., eds. Pharmacology and functional regulation of dopaminergic neurons: Proceedings of a satellite symposium of the IUPHAR 10th International Congress of Pharmacology, 31 August-2 September 1987. Littleton, Mass: PSG Pub. Co., 1988.

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9

M, Beart P., Woodruff Geoffrey N, Jackson D. M, International Union of Pharmacology y International Congress of Pharmacology (10th : 1987 : Cessnock, N.S.W.), eds. Pharmacology and functional regulation of dopaminergic neurons: Proceedings of a satellite symposium of the IUPHAR 10th International Congress of Pharmacology, 31 August-2 September 1987. Houndmills, Basingstoke, Hampshire: Macmillan Press, Scientific & Medical, 1988.

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10

W, Stone T., ed. CNS neurotransmitters and neuromodulators: Dopamine. Boca Raton: CRC Press, 1996.

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11

W, Stone T., ed. CNS neurotransmitters and neuromodulators: Glutamate. Boca Raton: CRC Press, 1995.

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12

Triarhou, Lazaros C. Dopaminergic Neuron Transplantation in the Weaver Mouse Model of Parkinson’s Disease. Boston, MA: Springer US, 2002. http://dx.doi.org/10.1007/978-1-4615-0699-7.

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13

Dong, Jing-fei. Morphological and biochemical characterization of human second trimester foetal dopaminergic neurones and identification of factors influencing their survival and preservation in vitro: A study related to clinical neural transplantation for Parkinson's disease. Wolverhampton: University of Wolverhampton, 1993.

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14

Beart, P. Dopaminergic Neurons. Palgrave Macmillan, 1988.

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15

(Editor), D. M. Jackson, ed. Pharmacology and Functional Regulation of Dopaminergic Neurons. Mosby-Year Book, 1989.

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16

Esposito, Ennio, Vincenzo Di Matteo y Giuseppe di Giovanni. Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Springer, 2012.

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17

Esposito, Ennio, Vincenzo Di Matteo y Giuseppe di Giovanni. Birth, Life and Death of Dopaminergic Neurons in the Substantia Nigra. Springer, 2011.

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18

Triarhou, Lazaros C. Dopaminergic Neuron Transplantation in the Weaver Mouse Model of Parkinson's Disease. Springer London, Limited, 2012.

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19

Dopaminergic Neuron Transplantation in the Weaver Mouse Model of Parkinson's Disease. Springer, 2003.

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20

Triarhou, Lazaros C. Dopaminergic Neuron Transplantation in the Weaver Mouse Model of Parkinson's Disease. Springer, 2012.

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21

Beninger, Richard J. Neuroanatomy and dopamine systems. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0011.

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Neuroanatomy and dopamine systems explains how sensory signals ascend the central nervous system via a series of nuclei; axons detecting specific elements converge onto higher-order neurons that respond to particular stimulus features. Assemblies of feature-detection cells in the cerebral cortex detect complex stimuli such as faces. These cell assemblies project to motor nuclei of the dorsal and ventral striatum where they terminate on dendritic spines of efferent medium spiny neurons. Dopaminergic projections from ventral mesencephalic nuclei terminate on the same spines. Individual corticostriatal afferents contact relatively few medium spiny neurons and individual dopaminergic neurons contact a far larger number. Stimuli activate specific subsets of corticostriatal synapses. Synaptic activity that is closely followed by a rewarding stimulus, that produces a burst of action potentials in dopaminergic neurons, is modified so that those specific corticostriatal synapses acquire an increased ability to elicit approach and other responses in the future, i.e., incentive learning.
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22

Beninger, Richard J. Dopamine and the elements of incentive learning. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0003.

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Dopamine and the elements of incentive learning explains how, in lever pressing for food tasks, incentive learning produces a gradient of attractiveness of environment stimuli: during magazine training, food activates dopaminergic neurons and the click and food cup become conditioned incentive stimuli, acquiring the ability to elicit approach and other responses; during lever-press training, the click activates dopaminergic neurons and the lever and lever-related stimuli become conditioned incentive stimuli. In conditioned place preference, amphetamine enhances dopaminergic neurotransmission and stimuli paired with amphetamine become conditioned incentive stimuli. In conditioned activity experiments, test-box stimuli paired with a dopamine-enhancer, e.g., cocaine, produce greater activity revealing incentive learning. In conditioned avoidance, the offset of an aversive warning stimulus putatively activates dopaminergic neurons leading safety-related stimuli to become conditioned incentive stimuli. If trained animals are treated with a dopamine receptor blocker, the initially intact ability of conditioned incentive stimuli to control responding declines over trials.
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23

Beninger, Richard J. Schizophrenia, Parkinson’s disease, and attention deficit hyperactivity disorder. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0009.

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Schizophrenia, Parkinson’s disease, and attention deficit hyperactivity disorder (ADHD) discusses how hyperactive dopaminergic neurotransmission appears to underlie schizophrenia’s positive symptoms, loss of dopaminergic neurons in adulthood leads to Parkinson’s disease, and dopamine neuron hypofunction in childhood and adolescence may underlie ADHD. Positive schizophrenia symptoms may arise from excessive incentive learning that is gradually lost with antipsychotic treatment. Declarative learning and memory may contribute to delusions based on excessive incentive learning. Loss of responsiveness to environmental stimuli in Parkinson’s may result from a decrease of their conditioned incentive value and inverse incentive learning. Conditioned incentive stimuli not encountered while in a state of decreased dopaminergic neurotransmission may retain their incentive value, producing apparent kinesia paradoxa. Dopamine hypofunction in juveniles does not lead to hypokinesia but may result in loss of incentive learning that focuses attention. Pro-dopaminergic drugs have a calming effect in ADHD, presumably because they reinstate normal incentive learning.
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24

Triarhou, Lazaros C. Dopaminergic Neuron Transplantation in the Weaver Mouse Model of Parkinson's Disease (Advances in Experimental Medicine and Biology, 517). Kluwer Academic/Plenum Publishers, 2002.

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25

Rosemary Eleonor Anne.* Craig. Dopamine metabolism in pregnancy: impact of amino acid supplementation on regional dopaminergic neurons in dams and fetuses. 1989.

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26

Chiara, Gaetano Di. Dopamine in the CNS I. Springer London, Limited, 2012.

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27

Dopamine in the CNS I. Springer, 2002.

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28

Chiara, Gaetano Di. Dopamine in the CNS I. Springer Berlin / Heidelberg, 2012.

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29

Dopamine in the CNS I. Springer, 2011.

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30

Beninger, Richard J. Drug abuse and incentive learning. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0010.

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Drug abuse and incentive learning explains how abused drugs, including nicotine, ethanol, marijuana, amphetamine, cocaine, morphine, and heroin, produce conditioned place preference and are self-administered; dopamine receptor antagonists block these effects. Stimuli that become reliable predictors of drug reward produce burst firing in dopaminergic neurons, but the drug retains its ability to activate dopaminergic neurons. Thus, repeated drug users experience two activations of dopaminergic neurotransmission, one upon exposure to the conditioned stimuli signaling the drug and another upon taking the drug. This may lead to long-term neurobiological changes that contribute to withdrawal and addiction. Withdrawal can be remediated by abstinence but this does not reduce the conditioned incentive value of cues associated with drug taking; those cues can lead to relapse. Effective treatment will include detoxification and systematic exposure to drug taking-associated conditioned incentive stimuli in the absence of drug so that those stimuli lose their ability to control responses.
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31

Walsh, Richard A. Smoothing out the Ups and Downs. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0001.

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The progressive loss of nigrostriatal dopaminergic neurons with advancing disease exposes the trough between every dose of levodopa in Parkinson’s disease. This is due to the combination of a loss of native dopamine production to fill in this interdose interval and a reduction in dopaminergic terminals to take up and release dopamine long beyond its short plasma half-life. The clinical result is wearing off—an awareness in patients of returning symptomatology while waiting for their next dose. Where consistent and impacting negatively on function on any level, there are a number of initial oral approaches to smooth out dopaminergic stimulation before more invasive advanced therapeutic options need to be considered.
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32

Beninger, Richard J. Life's rewards. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.001.0001.

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Life’s Rewards: Linking Dopamine, Incentive Learning, Schizophrenia, and the Mind explains how increased brain dopamine produces reward-related incentive learning, the acquisition by neutral stimuli of increased ability to elicit approach and other responses. Dopamine decreases may produce inverse incentive learning, the loss by stimuli of the ability to elicit approach and other responses. Incentive learning is gradually lost when dopamine receptors are blocked. The brain has multiple memory systems defined as “declarative” and “non-declarative;” incentive learning produces one form of non-declarative memory. People with schizophrenia have hyperdopaminergia, possibly producing excessive incentive learning. Delusions may rely on declarative memory to interpret the world as it appears with excessive incentive learning. Parkinson’s disease, associated with dopamine loss, may involve a loss of incentive learning and increased inverse incentive learning. Drugs of abuse activate dopaminergic neurotransmission, leading to incentive learning about drug-associated stimuli. After withdrawal symptoms have been alleviated by detoxification treatment, drug-associated conditioned incentive stimuli will retain their ability to elicit responses until they are repeatedly experienced in the absence of primary drug rewards. Incentive learning may involve the action of dopamine at dendritic spines of striatal medium spiny neurons that have recently had glutamatergic input from assemblies of cortical neurons activated by environmental and proprioceptive stimuli. Glutamate initiates a wave of phosphorylation normally followed by a wave of phosphatase activity. If dopaminergic neurons fire, stimulation of D1 receptors prolongs the wave of phosphorylation, allowing glutamate synaptic strengthening. Activity in dopaminergic neurons in humans appears to affect mental experience.
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33

(Editor), Howard J. Federoff, Robert E. Burke (Editor), Stanley Fahn (Editor) y Gary Fiskum (Editor), eds. Parkinson's Disease: The Life Cycle of the Dopamine Neuron (Annals of the New York Academy of Sciences, V. 991). New York Academy of Sciences, 2003.

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34

Beninger, Richard J. Dopamine as the dependent variable. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0005.

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Dopamine as the dependent variable discusses how postmortem biochemistry, intracerebral microdialysis, electrophysiological recording, in vivo electrochemistry, and positron emission tomography studies provide compelling evidence that dopaminergic neurons are activated by primary rewarding stimuli including food and water and by numerous conditioned incentives, including money. Early in training, primary rewarding stimuli activate dopaminergic neurons. When a cue is reliably paired with a primary rewarding stimulus over trials, the dopamine response begins to be seen upon presentation of the cue and eventually is not seen upon presentation of the primary rewarding stimulus when it follows the cue. These conditioned cues acquire the ability to act as rewarding stimuli that can produce incentive learning. If conditioned incentive stimuli are repeatedly presented in the absence of primary incentive stimuli, they gradually lose their ability to elicit approach and other responses and to act as rewarding stimuli by producing incentive learning in their own right.
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35

L, Iversen Leslie, ed. Dopamine handbook. New York: Oxford University Press, 2010.

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36

Beninger, Richard J. Introduction. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0001.

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The Introduction provides a brief overview of the book. The central theme is dopamine-mediated reward-related incentive learning—the acquisition by neutral stimuli of an increased ability to elicit approach and other responses. The brain has multiple memory systems defined as “declarative” and “non-declarative”; incentive learning produces one form of non-declarative memory. Once incentive learning is established it is gradually lost when the rewarding stimulus is no longer available or when dopamine function is reduced. Decreases in dopaminergic neurotransmission may produce inverse incentive learning—the loss by stimuli of their ability to elicit approach and other responses. Dopamine-related diseases including schizophrenia, Parkinson’s, attention deficit hyperactivity disorder, and drug abuse involve altered incentive learning. Incentive and inverse incentive learning may occur by the actions of dopamine, adenosine, and endocannabinoids at dendritic spines of striatal medium spiny neurons that have had recent glutamate input. Activity in dopaminergic neurons in humans appears to affect mental experience.
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37

Walsh, Richard A. “I Am Not Sure If I Should Do DaT”. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0008.

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Nuclear medicine-based imaging techniques can provide an estimation of nigrostriatal tract denervation based on radionucleotide uptake in the distal presynaptic terminals of dopaminergic neurons. Although unhelpful in differentiating between differing etiologies of denervation in varied neurodegenerative disorders associated with parkinsonism, this imaging is justified in situations in which parkinsonism is believed to be drug-induced or functional or in cases in which subclinical parkinsonism is suspected. The most common clinical situation in which dopamine transporter imaging is helpful is in the patient on neuroleptic therapy that cannot be stopped who has developed parkinsonism. Dopamine transporter imaging should be normal in drug-induced tremor.
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38

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Neuroactive Steroids (CNS Neurotransmitters & Neuromodulators). CRC, 1996.

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39

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Dopamine. CRC-Press, 1996.

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40

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. Taylor & Francis Group, 2020.

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41

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. CRC, 1994.

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42

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Glutamate. CRC, 1995.

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43

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. Taylor & Francis Group, 2020.

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44

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. Taylor & Francis Group, 2020.

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45

Stone, Trevor W. CNS Neurotransmitters and Neuromodulators: Acetylcholine. Taylor & Francis Group, 2020.

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