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      The molecular biology of memory: cAMP, PKA, CRE, CREB-1, CREB-2, and CPEB

      review-article
      Author(s): 1 ,
      Publication date (Electronic):
      Journal: Molecular Brain
      Publisher: BioMed Central

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          Abstract

          The analysis of the contributions to synaptic plasticity and memory of cAMP, PKA, CRE, CREB-1, CREB-2, and CPEB has recruited the efforts of many laboratories all over the world. These are six key steps in the molecular biological delineation of short-term memory and its conversion to long-term memory for both implicit (procedural) and explicit (declarative) memory. I here first trace the background for the clinical and behavioral studies of implicit memory that made a molecular biology of memory storage possible, and then detail the discovery and early history of these six molecular steps and their roles in explicit memory.

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          The molecular biology of memory storage: a dialogue between genes and synapses.

          E R Kandel (2001)
          One of the most remarkable aspects of an animal's behavior is the ability to modify that behavior by learning, an ability that reaches its highest form in human beings. For me, learning and memory have proven to be endlessly fascinating mental processes because they address one of the fundamental features of human activity: our ability to acquire new ideas from experience and to retain these ideas over time in memory. Moreover, unlike other mental processes such as thought, language, and consciousness, learning seemed from the outset to be readily accessible to cellular and molecular analysis. I, therefore, have been curious to know: What changes in the brain when we learn? And, once something is learned, how is that information retained in the brain? I have tried to address these questions through a reductionist approach that would allow me to investigate elementary forms of learning and memory at a cellular molecular level-as specific molecular activities within identified nerve cells.
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            Loss of recent memory after bilateral hippocampal lesions.

            W SCOVILLE, B Milner (1957)
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              Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path.

              T Bliss, T. Lomo (1973)
              1. The after-effects of repetitive stimulation of the perforant path fibres to the dentate area of the hippocampal formation have been examined with extracellular micro-electrodes in rabbits anaesthetized with urethane.2. In fifteen out of eighteen rabbits the population response recorded from granule cells in the dentate area to single perforant path volleys was potentiated for periods ranging from 30 min to 10 hr after one or more conditioning trains at 10-20/sec for 10-15 sec, or 100/sec for 3-4 sec.3. The population response was analysed in terms of three parameters: the amplitude of the population excitatory post-synaptic potential (e.p.s.p.), signalling the depolarization of the granule cells, and the amplitude and latency of the population spike, signalling the discharge of the granule cells.4. All three parameters were potentiated in 29% of the experiments; in other experiments in which long term changes occurred, potentiation was confined to one or two of the three parameters. A reduction in the latency of the population spike was the commonest sign of potentiation, occurring in 57% of all experiments. The amplitude of the population e.p.s.p. was increased in 43%, and of the population spike in 40%, of all experiments.5. During conditioning at 10-20/sec there was massive potentiation of the population spike (;frequency potentiation'). The spike was suppressed during stimulation at 100/sec. Both frequencies produced long-term potentiation.6. The results suggest that two independent mechanisms are responsible for long-lasting potentiation: (a) an increase in the efficiency of synaptic transmission at the perforant path synapses; (b) an increase in the excitability of the granule cell population.
              Article 0 comments Cited 505 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Mol Brain
                Journal ID (iso-abbrev): Mol Brain
                Title: Molecular Brain
                Publisher: BioMed Central
                ISSN (Electronic): 1756-6606
                Publication date Collection: 2012
                Publication date (Electronic): 14 May 2012
                Volume: 5
                Page: 14
                Affiliations
                [1 ]Department of Neuroscience, Columbia University, 1051 Riverside Drive, #664, New York, NY, 10032, USA
                Article
                Publisher ID: 1756-6606-5-14
                DOI: 10.1186/1756-6606-5-14
                PMC ID: 3514210
                PubMed ID: 22583753
                SO-VID: 3b2b1c6b-18a8-40d8-849f-41aeaafc2e45
                Copyright © Copyright ©2012 Kandel; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 22 February 2012
                Date accepted : 18 April 2012
                Categories
                Subject: Review

                ScienceOpen disciplines: Neurosciences
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                ScienceOpen disciplines: Neurosciences

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