In search of cellular mechanisms of memory

Matthies, H

doi:10.1016/0301-0082(89)90024-5

Cited by 197 publications

(100 citation statements)

References 231 publications

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“…CBP⌬1 transgenic mice show a specific deficit in long-term memory (LTM), but intact short-term memory (STM), following contextual fear conditioning. This result agrees with extensive evidence that LTM, but not STM, requires the transcription and translation of new proteins (Davis and Squire 1984;Matthies 1989). Perhaps surprisingly, no impairment was observed following cued fear conditioning.…”

supporting

confidence: 91%

What's right with my mouse model? New insights into the molecular and cellular basis of cognition from mouse models of Rubinstein-Taybi Syndrome: Table 1.

Josselyn¹

2005

Learn. Mem.

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supporting

confidence: 91%

What's right with my mouse model? New insights into the molecular and cellular basis of cognition from mouse models of Rubinstein-Taybi Syndrome: Table 1.

Josselyn¹

2005

Learn. Mem.

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“…LTP/LTD maintenance requires the synthesis of plasticity-related proteins (PRPs) (Krug et al, 1984;Frey et al, 1988;Matthies, 1989;Otani et al, 1989;Manahan-Vaughan et al, 2000). How PRPs interact only with activated synapses expressing LTP or LTD is fundamental to synapse specificity of the process and can be explained by the "synaptic tagging" hypothesis .…”

Section: Introductionmentioning

confidence: 99%

Identification of Compartment- and Process-Specific Molecules Required for “Synaptic Tagging” during Long-Term Potentiation and Long-Term Depression in Hippocampal CA1

Sajikumar

Navakkode

Frey³

2007

J. Neurosci.

188

230

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Protein synthesis-dependent forms of hippocampal long-term potentiation (late LTP) and long-term depression (late LTD) are prominent cellular mechanisms underlying memory formation. Recent data support the hypothesis that neurons store relevant information in dendritic functional compartments during late LTP and late LTD rather than in single synapses. It has been suggested that processes of "synaptic tagging" are restricted to such functional compartments. Here, we show that in addition to apical CA1 dendrites, synaptic tagging also takes place within basal CA1 dendritic compartments after LTP induction. We present data that tagging in the basal dendrites is restricted to these compartments. Plasticity-related proteins, partially nonspecific to the locally induced process, are synthesized in dendritic compartments and then captured by local, process-specific synaptic tags. We support these findings in two ways: (1) late LTP/LTD, locally induced in apical or basal (late LTP) dendrites of hippocampal CA1 neurons, does not spread to the basal or apical compartment, respectively; (2) the specificity of the synaptic plasticity event is achieved by the activation of process-and compartmentspecific synaptic tag molecules. We have identified calcium/calmodulin-dependent protein kinase II as the first LTP-specific and extracellular signal-regulated kinase 1/2 as LTD-specific tag molecules in apical dendritic CA1 compartments, whereas either protein kinase A or protein kinase M mediates LTP-specific tags in basal dendrites.

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“…Inhibition of protein synthesis during each of these phases was am-nesic (for review, see Matthies 1989). These findings suggested that the synthesis of proteins necessary for consolidation of the memory trace may be under the control of early induced regulatory proteins.…”

Section: Introductionmentioning

confidence: 99%

Suppression of c-fos induction in rat brain impairs retention of a brightness discrimination reaction.

Grimm¹,

Schicknick²,

Riede³

et al. 1997

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IntroductionRecently, the induction of transcription factor-encoding immediate-early genes such as c-fos was observed in distinct brain regions of rats trained to acquire a footshock-motivated brightness discrimination in a Y-maze. The functional relevance of inducible transcription factors for learning and memory formation is, however, not clear. To address this question in the present study, we have used a synthetic antisense phosphorothioate oligodeoxynucleotide to suppress in vivo the expression of c-fos in rat brain.

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In search of cellular mechanisms of memory

Cited by 197 publications

References 231 publications

What's right with my mouse model? New insights into the molecular and cellular basis of cognition from mouse models of Rubinstein-Taybi Syndrome: Table 1.

What's right with my mouse model? New insights into the molecular and cellular basis of cognition from mouse models of Rubinstein-Taybi Syndrome: Table 1.

Identification of Compartment- and Process-Specific Molecules Required for “Synaptic Tagging” during Long-Term Potentiation and Long-Term Depression in Hippocampal CA1

Suppression of c-fos induction in rat brain impairs retention of a brightness discrimination reaction.

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