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Deficient long-term memory in mice with a targeted mutation of the cAMP-responsive element-binding protein

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TLDR
Consistent with models claiming a role for long-term potentiation (LTP) in memory, LTP in hippocampal slices from CREB mutants decayed to baseline 90 min after tetanic stimulation, however, paired-pulse facilitation and posttetanic potentiation are normal.
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This article is published in Cell.The article was published on 1994-10-07. It has received 1832 citations till now. The article focuses on the topics: CAMP Responsive Element Binding Protein & Neuronal memory allocation.

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Emotion Circuits in the Brain

TL;DR: The field of neuroscience has, after a long period of looking the other way, again embraced emotion as an important research area, and much of the progress has come from studies of fear, and especially fear conditioning as mentioned in this paper.
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The Molecular Biology of Memory Storage: A Dialogue Between Genes and Synapses

TL;DR: This book aims to investigate elementary forms of learning and memory at a cellular molecular level—as specific molecular activities within identified nerve cells withinidentified nerve cells.
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Morris water maze: procedures for assessing spatial and related forms of learning and memory

TL;DR: The Morris water maze has proven to be a robust and reliable test that is strongly correlated with hippocampal synaptic plasticity and NMDA receptor function and trial-dependent, latent and discrimination learning can be assessed using modifications of the basic protocol.
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Transcriptional regulation by the phosphorylation-dependent factor CREB

TL;DR: The transcription factor CREB functions in glucose homeostasis, growth-factor-dependent cell survival, and has been implicated in learning and memory, and how is specificity achieved in these signalling pathways?
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Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval

TL;DR: It is shown that consolidated fear memories, when reactivated during retrieval, return to a labile state in which infusion of anisomycin shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivation was performed 1 or 14 days after conditioning.
References
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A synaptic model of memory: long-term potentiation in the hippocampus

TL;DR: The best understood form of long-term potentiation is induced by the activation of the N-methyl-d-aspartate receptor complex, which allows electrical events at the postsynaptic membrane to be transduced into chemical signals which, in turn, are thought to activate both pre- and post Synaptic mechanisms to generate a persistent increase in synaptic strength.
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Place navigation impaired in rats with hippocampal lesions.

TL;DR: It is reported that, in addition to a spatial discrimination impairment, total hippocampal lesions also cause a profound and lasting placenavigational impairment that can be dissociated from correlated motor, motivational and reinforcement aspects of the procedure.
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Memory and the hippocampus: A synthesis from findings with rats, monkeys, and humans.

TL;DR: The role of the hippocampus is considered, which is needed temporarily to bind together distributed sites in neocortex that together represent a whole memory.
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Differential Contribution of Amygdala and Hippocampus to Cued and Contextual Fear Conditioning

TL;DR: An associative roles for the amygdala and a sensory relay role for the hippocampus are suggested in fear conditioning, which is involved in the conditioning of fear responses to simple, modality-specific conditioned stimuli as well as to complex, polymodal stimuli.
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Spatial Localization Does Not Require the Presence of Local Cues

TL;DR: It is demonstrated that rats can rapidly learn to locate an object that they can never see, hear, or smell provided it remains in a fixed spatial location relative to distal room cues.
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