Books on the topic 'Hippocampal System'

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1

Howard, Eichenbaum, ed. Memory, amnesia, and the hippocampal system. Cambridge, Mass: MIT Press, 1993.

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2

Gray, Jeffrey Alan. The neuropsychology of anxiety: An enquiry into the functions of the septo-hippocampal system. Oxford: Clarendon Press, 1986.

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3

Gray, Jeffrey Alan. The neuropsychology of anxiety: An enquiry into the functions of the septo-hippocampal system. 2nd ed. Oxford: Oxford University Press, 2000.

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4

Yi, Chae-wŏn. Sinʼgyŏng toksŏng mulchil ŭi toksŏng chagyong yŏnghyang yŏnʼgu =: Effects of organic solvent in neural stem cell and hippocampal neuron. [Seoul]: Sikpʻum Ŭiyakpʻum Anjŏnchʻŏng, 2007.

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5

Hannula, Deborah E., and Melissa C. Duff, eds. The Hippocampus from Cells to Systems. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-50406-3.

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6

Taupin, Philippe. The hippocampus: Neurotransmission and plasticity in the nervous system. New York: Nova Biomedical Books, 2007.

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7

1951-, Miles Richard, ed. Neuronal networks of the hippocampus. Cambridge: Cambridge University Press, 1991.

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8

Milford, Michael John. Robot navigation from nature: Simultaneous localisation, mapping, and path planning based on hippocampal models. Berlin: Springer, 2008.

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9

1935-, Okada Yashuiro, Nihon Shinkei Kagaku Kyōkai, Burein Saiensu Shinkō Zaidan (Japan), and Nihon Shinkei Kagaku Kyōkai. Meeting, eds. The role of adenosine in the nervous system: Proceedings of the International Symposium on Adenosine in the Nervous System, July 13-16, 1996, Kobe, Japan. Amsterdam: Elsevier, 1997.

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10

Staff, CIBA Foundation Symposium. Functions of the Septo-Hippocampal System. Wiley & Sons, Limited, John, 2008.

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11

Whelan, Julie, and Katherine Elliott. Functions of the Septo-Hippocampal System. Wiley & Sons, Incorporated, John, 2009.

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12

Cohen, Neal J. Memory, amnesia and the hippocampal system. Bradford Books, 1996.

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13

Song, Dong, and Theodore W. Berger. Hippocampal memory prosthesis. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780199674923.003.0055.

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Damage to the hippocampus and surrounding regions of the medial temporal lobe can result in a permanent loss of the ability to form new long-term memories. Hippocampal memory prosthesis is designed to restore this ability. The animal model described here is the memory-dependent, delayed nonmatch-to-sample (DNMS) task in rats, and the core of the prosthesis is a biomimetic multi-input, multi-output (MIMO) nonlinear dynamical model that predicts hippocampal output (CA1) signals based on input (CA3) signals. When hippocampal CA1 function is pharmacologically blocked, successful DNMS behavior is abolished. However, when MIMO model predictions are used to re-instate CA1 memory-related activities with electrical stimulation, successful DNMS behavior and long-term memory function are restored. The hippocampal memory prosthesis has been successfully implemented in rodents and nonhuman primates, but the current system requires major advances before it can approach a working prosthesis. Looking forward, a deeper knowledge of neural coding will provide further insights.
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14

Gray, Jeffrey A. The Neuropsychology of Anxiety: An Enquiry into the Functions of the Septo-Hippocampal System (Oxford Psychology). Oxford University Press, USA, 1987.

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15

The Neuropsychology of Anxiety: An Enquiry into the Functions of the Septo-Hippocampal System (Oxford Psychology Series). Oxford University Press, USA, 2003.

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16

Beninger, Richard J. Multiple memory systems. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198824091.003.0004.

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Multiple memory systems describes how memories can be declarative or non-declarative; incentive learning produces one type of non-declarative memory. Patients with bilateral hippocampal damage have declarative memory deficits (amnesia) but intact non-declarative memory; patients with striatal dysfunction, for example, Parkinson’s patients who lose striatal dopamine have impaired incentive learning but intact declarative memory. Rats with lesions of the fornix (hippocampal output pathway), but not lesions of the dorsal striatum, have impaired spatial (declarative) memory; rats with lesions of the dorsal striatum, but not fornix, have impaired stimulus–response memory that relies heavily on incentive learning. These memory systems possibly inhibit one another to control responding: in rats, a group that received fornix lesions and had impaired spatial learning did better on an incentive task; in humans, hippocampus damage was associated with improvement on an incentive learning task and striatal damage was associated with increased involvement of the hippocampus in a route-recognition task.
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17

Fisch, Adam. Limbic and Olfactory Systems. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199845712.003.0276.

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Chapter 21 discusses the limbic and olfactory systems, including parts 1 and 2 of the limbic system, the anatomy and circuitry of the hippocampus, parts 1 and 2 of the olfactory system, and parts 1 and 2 of the olfactory cortex and basal forebrain.
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18

Attems, Johannes, and Kurt A. Jellinger. Neuropathology. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0006.

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This chapter describes the main neuropathological features of the most common age associated neurodegenerative diseases including Alzheimer's disease, Parkinson's disease and dementia with Lewy bodies as well as other less frequent ones such as multiple system atrophy, Pick's disease, corticobasal degeneration, progressive supranuclear palsy, argyrophilic grain disease, neurofibrillary tangle dominant dementia, frontotemporal lobar degeneration with TDP-43 pathology and Huntington's disease. Likewise cerebral amyloid angiopathy, hippocampal sclerosis, vascular dementia and prion diseases are described. A main aim of this chapter is to assist the reader in interpreting neuropathological reports, hence criteria for the neuropathological classifications of the major diseases are provided. One section covers general considerations on neurodegeneration and basic pathophysiological mechanisms of tau, amyloid-β, α-synuclein, TDP-43 and prions are briefly described in the sections on the respective diseases. Finally, one section is dedicated to cerebral multimorbidity and we give a view on currently emerging neuropathological methods.
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19

Neuronal Networks of the Hippocampus. Cambridge University Press, 2008.

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20

Traub, Roger D., and Richard Miles. Neuronal Networks of the Hippocampus. Cambridge University Press, 2012.

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21

(Editor), L. W. Swanson, ed. Integrated Systems of the CNS, Part I: Hypothalamus, Hippocampus, Amygdala, Retina (Handbook of Chemical Neuroanatomy). Elsevier Science Pub Co, 1987.

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22

Milford, Michael John. Robot Navigation from Nature: Simultaneous Localisation, Mapping, and Path Planning Based on Hippocampal Models. Springer London, Limited, 2007.

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23

Milford, Michael John. Robot Navigation from Nature: Simultaneous Localisation, Mapping, and Path Planning Based on Hippocampal Models. Springer, 2010.

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24

Wang, Zheng. Reduction of glutamate- and tyrosine hydroxylase-like immunoreactivities in the locus coeruleus neurons following repetitive injection of [beta]-amyloid into hippocampus of the rat. 1993.

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25

Hannula, Deborah E., and Melissa C. Duff. Hippocampus from Cells to Systems: Structure, Connectivity, and Functional Contributions to Memory and Flexible Cognition. Springer International Publishing AG, 2017.

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26

Hannula, Deborah E., and Melissa C. Duff. The Hippocampus from Cells to Systems: Structure, Connectivity, and Functional Contributions to Memory and Flexible Cognition. Springer, 2018.

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27

Joseph, R. Gabriel. Limbic System : Amygdala, Hypothalamus, Septal Nuclei, Cingulate, Hippocampus: Emotion, Memory, Language, Development, Evolution, Love, Attachment, ... Aggression, Dreams, Hallucinations, Amnesia. Science Publishers, 2017.

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28

Joseph, R. Gabriel. Limbic System : Amygdala, Hypothalamus, Septal Nuclei, Cingulate, Hippocampus: Emotion, Memory, Language, Development, Evolution, Love, Attachment, ... Hallucinations, Amnesia, Abnormal Behavior. Science Publishers, 2017.

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29

Shea, Nicholas. Structural Correspondence. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198812883.003.0005.

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Structural correspondence is the other exploitable relation that figures in our case studies. It is found in the cognitive map realized by place cells in the hippocampus. When an exploitable structural correspondence is exploited in the service of a system’s performance of its task functions, it is thereby constituted as a UE structural correspondence. In some cases where there is a superficially attractive structural correspondence, it can turn out that the correspondence is not being made use of; indeed, that structural representation does not arise. These cases are contrasted with two further cases where an exploitable structural correspondence is exploited. A structural correspondence may hold only approximately. That notion is defined and put to work.
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30

O’Flaherty, Brendan M., Chia-Chun Hsu, M. Anzar Abbas, and Donald G. Rainnie. Cellular Physiology of the Basolateral Complex of the Amygdala and Its Modulation by Stress. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0003.

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Fear is a critical emotional response that allows an organism to safely navigate through dangerous environments. The neural systems underlying the fear response have been well characterized, and include the amygdala, hippocampus, prefrontal cortex, bed nucleus of stria terminalis, nucleus accumbens, and others. While normally these brain regions coordinate to produce an appropriate fear response, the fear network in humans can become dysregulated after a traumatic event. The resulting phenotype of hyperarousal, avoidance, and re-experiencing of fear known as post-traumatic stress disorder (PTSD) is a growing problem in the United States. This chapter focuses on the role of the basolateral complex (BLC) of the amygdala, which has been implicated in the neuropathology of PTSD, particularly the hyperarousal, fear generalization, and fear extinction deficits characteristic of the disorder, as well as aspects of the microcircuitry, network connectivity, and neuromodulation of the BLC that may be involved in the pathophysiology of PTSD.
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31

Cellular and Molecular Neurobiology. Academic Pr, 1996.

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32

Cellular and Molecular Neurobiology (Deluxe Edition). Academic Press, 2001.

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33

Hammond, Constance. Cellular and Molecular Neurobiology. Elsevier Science & Technology Books, 2012.

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34

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