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ScienceWeek
NEUROBIOLOGY: ON THE HIPPOCAMPUS AND MEMORY
The following points are made by J.L. Lee et al (Science 2004 304:839):
1) The long-standing hypothesis of memory consolidation proposes that fragile, dynamic memory traces are converted into stable, long-term memory (LTM) gradually over time (1-3). Thus, internal representations of the external world eventually become encoded and stored as persistent molecular and/or structural modifications (4).
2) The central dogma of the permanence of LTM has been challenged by evidence showing the disruption of what are apparently fully consolidated memories when the memory is retrieved, or reactivated, immediately before treatment with various amnestic agents or in response to behavioral manipulations (5). The recall of a memory thus appears to place it into an active and labile state, from which it is reconsolidated back into an inactive and stable state (5).
3) This reconsolidation has been suggested, but not proven, to involve mechanisms similar to the consolidation process for the memory trace to be restabilized and its retrievability to be enhanced, or for new information to be incorporated into the old memory trace. This view is supported by the similarities in some of the cellular processes of consolidation and reconsolidation. Both are blocked by the protein synthesis inhibitor anisomycin, and both require the activation of the transcription factors CREB and Zif268. However, there are also differences in the temporal profile and susceptibility of memories to disruption after acquisition and retrieval, and reconsolidation does not engage all of the molecular mechanisms involved in consolidation.
4) In summary: The idea that new memories undergo a time-dependent consolidation process after acquisition has received considerable experimental support. More controversial has been the demonstration that established memories, once recalled, become labile and sensitive to disruption, requiring "reconsolidation" to become permanent. By infusing antisense oligodeoxynucleotides into the hippocampus of rats, the authors demonstrate that consolidation and reconsolidation are doubly dissociable component processes of memory. Consolidation involves brain-derived neurotrophic factor (BDNF) but not the transcription factor Zif268, whereas reconsolidation recruits Zif268 but not BDNF. The authors suggest these findings confirm a requirement for BDNF specifically in memory consolidation and also resolve the role of Zif268 in brain plasticity, learning, and memory.
References (abridged):
1. G. E. Mueller, A. Pilzecker, Z. Psychol. 1, 1 (1900)
2. D. O. Hebb, The Organization of Behavior (Wiley, New York, 1949)
3. J. L. McGaugh, Science 153, 1351 (1966)
4. E. R. Kandel, Science 294, 1030 (2001)
5. K. Nader, Trends Neurosci. 26, 65 (2003)
Science http://www.sciencemag.org
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Related Material:
MEMORY AND THE MEMORY CONSOLIDATION HYPOTHESIS
The following points are made by James L. McGaugh (Science 2000 287:248):
1) A century has passed since Georg Mueller (1850-1934) and Alfons Pilzecker proposed the perseveration-consolidation hypothesis of memory (1). In pioneering studies with human subjects, they found that memory of newly learned information was disrupted by the learning of other information shortly after the original learning and suggested that processes underlying new memories initially persist in a fragile state and consolidate over time. At the beginning of this new millennium, the consolidation hypothesis still guides research investigating the time-dependent involvement of neural systems and cellular processes enabling lasting memory (2-4).
2) Clinical evidence that cerebral trauma induces loss of recent memory was reported two decades before the publication of Mueller and Pilzecker's monograph, and shortly after its publication it was noted that the consolidation hypothesis provided an explanation for such retrograde amnesia (5). Ignored for almost half a century, the consolidation hypothesis was reinvigorated in 1949, when two papers reported that electroconvulsive shock induced retrograde amnesia in rodents, triggering a burst of studies of experimentally induced retrograde amnesia (2-4). That same year, Donald O. Hebb (1904-1985) and Ralph W. Gerard (1900-1974) proposed dual-trace theories of memory, suggesting that the stabilization of reverberating neural activity underlying short-term memory produces long-term memory.
3) The finding that protein synthesis inhibitors did not prevent the learning of tasks but disrupted memory of the training supports the view that there are (at least) two stages of memory and indicates that protein synthesis is required only for consolidation of long-term memory. The issue of whether short-and long-term memory (and, perhaps, other memory stages) are sequentially linked, as proposed by Hebb and Gerard, or act independently in parallel (3) remains central to current inquiry. The discovery that stimulant drugs administered within minutes or hours after training enhance memory consolidation further stimulated studies of memory consolidation (3). The use of treatments administered shortly after training to impair or enhance memory provides a highly effective and extensively used method of influencing memory consolidation without affecting either acquisition or memory retrieval.
4) In summary: The memory consolidation hypothesis proposed 100 years ago by Mueller and Pilzecker continues to guide memory research. The hypothesis that new memories consolidate slowly over time has stimulated studies revealing the hormonal and neural influences regulating memory consolidation, as well as molecular and cellular mechanisms.
References (abridged):
1. G. E. Mueller and A. Pilzecker, Z. Psychol. 1, 1 (1900)
2. S. E. Glickman, Psychol. Bull. 58, 218 (1961); J. L. McGaugh and M. J. Herz, Memory Consolidation (Albion, San Francisco, 1972); H. Weingartner and E. S. Parker, Eds., Memory Consolidation (Erlbaum, Hillsdale, NJ, 1984); H. A. Lechner, L. R. Squire, J. H. Byrne, Learn. Mem. 6, 77 (1999) [Free Full Text]; M. R. Polster, L. Nadel, D. L. Schacter, J. Cogn. Neurosci. 3, 95 (1991)
3. J. L. McGaugh, Science 153, 1351 (1966)
4. Y. Dudai, Neuron 17, 367 (1996)
5. T. Ribot, Diseases of Memory (Appleton, New York, 1882); W. McDougall, Mind 10, 388 (1901) ; W. H. Burnham, Am. J. Psychol. 14, 382 (1903)
Science http://www.sciencemag.org
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NEUROBIOLOGY: ON THE BIOLOGICAL BASIS OF MEMORY
Notes by ScienceWeek
Exactly 100 years ago, two psychologists, G.E. Mueller and A. Pilzecker, proposed what came to be called the perseveration-consolidation hypothesis of memory. In studies with human subjects, Mueller and Pilzecker found that memory of newly learned information was disrupted by the learning of other information shortly after the original learning, and they suggested that processes underlying new memories initially persist in a fragile state and then consolidate over time. This consolidation hypothesis still guides research, particularly research in neurobiology on the time-dependent involvement of neural systems and cellular processes enabling lasting memory.
At the present time, the concept of "synaptic plasticity" underlies nearly all theories of memories, the term referring to changes in the behavior of the junction (synapse) between two nerve cells resulting from past history.
Two prominent aspects of synaptic plasticity considered to be related to memory are "facilitation" and "potentiation". The term "facilitation" refers to a progressive increase in the amount of *neurotransmitter substance released at a synapse by successive nerve impulses (action potentials), the increase occurring during an input barrage consisting of repetitive stimulation (stimulus train). The term "potentiation" refers to an increase in neurotransmitter substance released by an action potential following repetitive stimulation of a synapse.
Both facilitation and potentiation can be long-lasting, and "long-term potentiation" has been a focus of much research on the cellular basis of memory, particularly in the hippocampus, a brain cortex structure in the medial part of the temporal lobe. In humans, among other functions, the hippocampus is apparently involved in short-term memory, and analysis of the neurological correlates of learning behavior in the rat indicates that the hippocampus of the rat is also involved in memory.
The following points are made by James L. McGaugh (Science 2000 287:248):
1) The author points out that the idea that synaptic mechanisms of long-term potentiation and long-term facilitation underlie memory remains a hypothesis.
2) The author points out that although studies of long-term potentiation and memory have focused on the involvement of the hippocampus, much evidence indicates that the hippocampus has only a time-limited role in the consolidation and/or stabilization of lasting memory.
3) The author points out that there are forms of memory that apparently do not involve the hippocampus and that may not use any known mechanisms of synaptic plasticity.
4) The author points out that despite theoretical conjectures, little is known about system and cellular processes mediating consolidation that continues for several hours or longer after learning, consolidation that creates lifelong memories.
Concerning the above caveats, the author concludes: "These issues remain to be addressed in this new century of research on memory consolidation."
Science http://www.sciencemag.org
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Notes by ScienceWeek:
neurotransmitter substance: Neurotransmitters are chemical substances released at the terminals of nerve axons in response to the propagation of an impulse to the end of that axon. The neurotransmitter substance diffuses into the synapse, the junction between the presynaptic nerve ending and the postsynaptic neuron, and at the membrane of the postsynaptic neuron the transmitter substance interacts with a receptor. Depending on the type of receptor, the result may be an excitatory or an inhibitory effect on the postsynaptic nerve cell.
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