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Books on the topic 'Hippocampal CA3'

Author: Grafiati

Published: 6 September 2023

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1

Ouanounou, Aviv. Modulation of synaptic transmission by exogenous calcium buffers in hippocampal CA1 neurons. Ottawa: National Library of Canada, 1996.

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2

Pawluski, Jodi Lynn. Primiparous rats, but not multiparous rats, exhibit dendritic atrophy in CA1 and CA3 pyramidal cells of the hippocampus. Ottawa: National Library of Canada, 2003.

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3

Breakwell, Nicholas Anthony. A1F[inferior 4]-induced synaptic plasticity in area CA1 of rat hippocampus. Birmingham: University of Birmingham, 1995.

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4

Wrong, Andrew D. Bimodal modulation of N-methyl-D-aspartate-induced currents in rat CA1 hippocampal neurons by kainate application. Ottawa: National Library of Canada, 2002.

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5

Jazayeri, Mehrdad. A theoretical investigation of the generation of a spontaneous slow rhythm in hippocampus Ca1. Ottawa: National Library of Canada, 2001.

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6

Dorri, Faramarz. Antisense deoxyoligonucleotide inhibitation of metabotropic glutamate receptor 5 synthesis in CA1 area of rat hippocampus. Ottawa: National Library of Canada, 1995.

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7

Donegan, Macayla. Coding of social novelty in the hippocampal Cornu Ammonis 2 region (CA2) and its disruption and rescue in a mouse model of schizophrenia. [New York, N.Y.?]: [publisher not identified], 2020.

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8

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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9

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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10

Maren, Stephen. Neural Circuits for Context Processing in Aversive Learning and Memory. Edited by Israel Liberzon and Kerry J. Ressler. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190215422.003.0005.

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The nature and properties of emotional expression depend importantly on not only the stimuli that elicit emotional responses, but also the context in which those stimuli are experienced. Deficits in context processing have been associated with a variety of cognitive-emotional disorders, including post-traumatic stress disorder (PTSD). These deficits can be localized to specific neural circuits underlying context processing in the mammalian brain. In particular, the hippocampus has been implicated through numerous animal and human studies to be involved both in normal contextual memory formation, but also in discrimination of trauma-related cues. Decreased hippocampal functioning, as is observed in PTSD, is associated with increased generalization of fear and threat responses as well as deficits in extinction of fear. Understanding context processing offers the opportunity to further understand the biology of PTSD and to target new approaches to therapeutics.

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11

Chen, Qiang Xiao. Intracellular calcium effects on the membrane currents of hippocampal CA1 neurons. 1991.

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12

Jalini, Shirin. Ischemia-induced changes in evoked glutamate release can be reduced by calcium buffering in hippocampal CA1 region. 2006.

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13

Gordon, Rupa Gupta, Melissa C. Duff, and Neal J. Cohen. Applications of Collaborative Memory: Patterns of Success and Failure in Individuals with Hippocampal Amnesia. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198737865.003.0023.

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A growing body of work suggests that collaboration can benefit memory. In our work on the neural substrates of collaborative learning, we find that many of these benefits extend even to individuals with profound memory impairment. We review this line of work highlighting the benefits and limits of collaborative learning in memory impaired populations. Understanding the contexts and circumstances of success and failure in collaborative learning in individuals with memory impairment advances scientific knowledge of how distinct forms of memory contribute to specific aspects of collaborative learning. Our discovery that memory-impaired individuals can benefit from collaborative learning under some conditions points to the promise of collaborative learning situations in the rehabilitation of memory and learning impairments.

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14

Weiner, J. L. Ethanol modulation of GABA[A]-mediated synaptic transmission in hippocampal CA1 neurons: A whole-cell patch-clamp study. 1994.

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15

Cherubini, Enrico, and Richard Miles, eds. The CA3 Region of the Hippocampus: How is it? What is it for? How does it do it? Frontiers Media SA, 2015. http://dx.doi.org/10.3389/978-2-88919-631-9.

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16

Hodgkiss, Andrew. Psychiatric consequences of cancer treatments: conventional chemotherapy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198759911.003.0006.

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The psychiatric consequences of a range of conventional chemotherapy agents are reviewed. Anti-folates can cause frank demyelination (methotrexate-induced leucoencephalopathy) or more subtle cognitive impairment. The latter is attributed to reduced hippocampal neurogenesis due to the excitotoxic effects of homocysteine. Low mood, due to reduced availability of SAM, is also found during anti-folate chemotherapy. Ifosfamide-induced encephalopathy is described. Depression and encephalopathies are found with mitotic spindle poisons. Procarbazine is considered as a monoamine oxidase inhibitor. Finally, the developing appreciation of the mixed neuropsychiatric actions of bexarotene, an RXR activator, is reviewed.

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17

Lleó, Alberto, and Rafael Blesa. Clinical course of Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0004.

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Alzheimer’s disease (AD) is an age-related neurodegenerative disorder, with onset usually in late life, characterized by progressive cognitive impairment, a variety of behavioural symptoms, and impairment in the activities of daily living. The initial symptom in typical AD is episodic memory loss, which reflects hippocampal dysfunction. The memory deficits are very characteristic with low recall performance despite retrieval facilitations with cueing. These initial deficits can be identified by appropriate cognitive tests. Behavioural symptoms can be present at early stages of the disease (even in pre-clinical states), although the frequency increases as the disease progresses. In the past decade there has been a growing interest in characterizing these pre-clinical and prodromal stages as treatments are expected to be more effective in these phases.

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18

LeBoutillier, Janelle Catherine. The effect of Ras/MAPK signaling in the mouse hippocampus: A morphological examination of synaptic and dendritic alterations in CA1 (California). 2004.

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19

Naninck, E. F. G., P. J. Lucassen, and Aniko Korosi. Consequences of Early-Life Experiences on Cognition and Emotion. Edited by Turhan Canli. Oxford University Press, 2013. http://dx.doi.org/10.1093/oxfordhb/9780199753888.013.003.

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Perinatal experiences during a critical developmental period program brain structure and function “for life,” thereby determining vulnerability to psychopathology and cognition in adulthood. Although these functional consequences are associated with alterations in HPA-axis activity and hippocampal structure and function, the underlying mechanisms remain unclear. The parent-offspring relationship (i.e., sensory and nutritional inputs by the mother) is key in mediating these lasting effects. This chapter discusses how early-life events, for example, the amount of maternal care, stress, and nutrition, can affect emotional and cognitive functions later in life. Interestingly, effects of perinatal malnutrition resemble the perinatal stress-induced long-term deficits. Because stress and nutrition are closely interrelated, it proposes that altered stress hormones and changes in specific key nutrients during critical developmental periods act synergistically to program brain structure and function, possibly via epigenetic mechanisms. Understanding how the adult brain is shaped by early experiences is essential to develop behavioural and nutritional preventive therapy.

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20

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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21

Gorman, Jack M. Making Connections. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190850128.003.0006.

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Although some functions, like speech and vision, can be linked to single, specific locations in the brain, complex emotions and behaviors usually involve complex interactions among brain regions. As our brains mature, these connections are shaped by our lived experiences. Scientists in basic neuroscience laboratories have traced the pathways and networks necessary for the acquisition, expression, and extinction of one emotion: fear. Brain imaging studies have shown that these same connected brain regions are activated by fear and anxiety in humans. The “fear network” includes the amygdala, hippocampus, and prefrontal cortex. Abnormalities in activity and strength of connections in the fear network are present in children and adults with anxiety disorders and depression. Brain networks that are necessary for other emotions and behaviors have been identified, so that today we look to how our brains are connected to understand our actions and emotions.

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22

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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23

Butz, Martin V., and Esther F. Kutter. Multisensory Interactions. Oxford University Press, 2017. http://dx.doi.org/10.1093/acprof:oso/9780198739692.003.0010.

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This chapter shows that multiple sensory information sources can generally be integrated in a similar fashion. However, seeing that different modalities are grounded in different frames of reference, integrations will focus on space or on identities. Body-relative spaces integrate information about the body and the surrounding space in body-relative frames of reference, integrating the available information across modalities in an approximately optimal manner. Simple topological neural population encodings are well-suited to generate estimates about stimulus locations and to map several frames of reference onto each other. Self-organizing neural networks are introduced as the basic computation mechanism that enables the learning of such mappings. Multisensory object recognition, on the other hand, is realized most effectively in an object-specific frame of reference – essentially abstracting away from body-relative frames of reference. Cognitive maps, that is, maps of the environment are learned by connecting locations over space and time. The hippocampus strongly supports the learning of cognitive maps, as it supports the generation of new episodic memories, suggesting a strong relation between these two computational tasks. In conclusion, multisensory integration yields internal predictive structures about spaces and object identities, which are well-suited to plan, decide on, and control environmental interactions.

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