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10 - A brain system for declarative memory
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- By Seth J. Ramus, Department of Psychology and Program in Neuroscience Bowdoin College Brunswick, ME 04011, Howard B. Eichenbaum, Director Cognitive Neurobiology Laboratory; Director Center for Memory and Brain; University Professor and Chairman Department of Psychology Boston University Center for Memory and Brain 2 Cummington Street Boston, MA 02215
- Edited by James R. Pomerantz, Rice University, Houston
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- Book:
- Topics in Integrative Neuroscience
- Published online:
- 08 August 2009
- Print publication:
- 21 February 2008, pp 265-298
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Summary
Our understanding about the brain system that mediates memory began in the 1950s with the landmark case study of patient HM (Scoville & Milner, 1957). To relieve epilepsy that was intractable to pharmacological intervention, surgeons removed a large part of this patient's temporal lobes, including the amygdala, part of the hippocampus, and the cortex immediately surrounding the hippocampus and amygdala. Following surgery, HM exhibited a severe amnesia, leaving nonmemory aspects of intelligence and cognition intact. This observation demonstrated that memory could be separated from other cognitive functions and that structures of the medial temporal lobe are critical to memory.
While the early neuropsychological reports clearly pointed to the importance of the temporal lobes in memory, there was debate over precisely which temporal structures were important. Because the available clinical cases did not provide highly specific anatomical resolution, efforts were made to develop animal models in which experimental brain lesions could be performed with the necessary anatomical specificity. However, the early efforts to model amnesia in monkeys and rats did not yield a consistent pattern of severe and selective amnesia, precluding useful insights into the anatomical identification of the memory system. With hindsight, it is now clear that the difficulty in characterizing the brain system responsible for memory arose for two reasons (Eichenbaum et al., 2000). First, while the memory deficit following medial temporal damage was initially thought to be global in nature, it is now understood that damage to the medial temporal region causes amnesia that is limited to a specific domain of memory, and that other brain systems mediate other types of memory.
17 - In Vivo Recording of Single Hippocampal Place Cells in Behaving Transgenic Mice
- Edited by Christian Hölscher, University of Oxford
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- Book:
- Neuronal Mechanisms of Memory Formation
- Published online:
- 13 October 2009
- Print publication:
- 06 November 2000, pp 407-426
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Summary
SUMMARY
In order to draw a closer connection between spatial memory and hippocampal long-term potentiation (LTP), the activity of a place cell that fires selectively when an animal is located in a certain area of a maze was examined in freely behaving knock-out mice that exhibit spatial learning deficit and altered hippocampal plasticity. This approach seeks to examine the effects of altered synaptic plasticity on the information coding mechanism by characterizing firing properties of certain hippocampal neurons directly underlying perception and memory. Available recording data indicated that synaptic plasticity in the hippocampus is not an essential mechanism for the formation of place selective firing of hippocampal pyramidal neurons, but is important for fine tuning and stabilizing its neural activity across time.
Together with genetic, pharmacologic, and in vitro electrophysiologic studies, this type of approach should allow us to examine whether experimental manipulations that block LTP change the capacity of neurons to process critical sensory stimuli and to code relevant cues into memory, and thus should provide a unique and promising avenue in bringing further insight into the cellular and physiologic mechanisms underlying learning and memory.
Introduction
A major focus of neuroscience research, and the central topic of this volume, is the identification of cellular and molecular plasticity mechanisms that mediate memory. Most studies aimed at this goal involve attempts to relate physiologic or molecular indices of neural plasticity to behavioral performance in learning and memory tests.