Discussion

Sossin, WS

doi:10.1016/0166-2236(96)20016-5

Cited by 39 publications

(4 citation statements)

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“…It is difficult, however, to know whether these new synapses are where memories are stored or whether they are a form of meta-plasticity providing a source of synapses that could become memory synapses in the future. We have argued that when a neuron is chosen as an Engram neuron it both strengthens inputs associated with the learning stimulus (tagged synapses) and generates new outputs to communicate the new information gained to new sources (Sossin, 1996 ). These new outputs would then be the source of new potential memory synapses when the memory is reactivated or associated with a new stimulus (Figure 1 ).…”

Section: Are Memory Synapses New Synapses?mentioning

confidence: 99%

Memory Synapses Are Defined by Distinct Molecular Complexes: A Proposal

Sossin

2018

Front. Synaptic Neurosci.

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Synapses are diverse in form and function. While there are strong evidential and theoretical reasons for believing that memories are stored at synapses, the concept of a specialized “memory synapse” is rarely discussed. Here, we review the evidence that memories are stored at the synapse and consider the opposing possibilities. We argue that if memories are stored in an active fashion at synapses, then these memory synapses must have distinct molecular complexes that distinguish them from other synapses. In particular, examples from Aplysia sensory-motor neuron synapses and synapses on defined engram neurons in rodent models are discussed. Specific hypotheses for molecular complexes that define memory synapses are presented, including persistently active kinases, transmitter receptor complexes and trans-synaptic adhesion proteins.

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Section: Are Memory Synapses New Synapses?mentioning

confidence: 99%

Memory Synapses Are Defined by Distinct Molecular Complexes: A Proposal

Sossin

2018

Front. Synaptic Neurosci.

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“…Pioneering studies in Aplysia showed that LTF generated by spaced training requires the activity of transcription factors belonging to the CREB family [31–34]. Moreover, not only is CREB required for long-term memory formation after spaced training, it is the rate-limiting step [35]. Thus, manipulating the CREB pathway such that a single stimulus or massed stimuli can activate CREB allows for long-term memory formation from these stimuli.…”

Section: Role Of Creb In Long-term Memory Formationmentioning

confidence: 99%

Molecular Determinants of the Spacing Effect

2012

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Long-term memory formation is sensitive to the pattern of training sessions. Training distributed over time (spaced training) is superior at generating long-term memories than training presented with little or no rest interval (massed training). This spacing effect was observed in a range of organisms from invertebrates to humans. In the present paper, we discuss the evidence supporting cyclic-AMP response element-binding protein 2 (CREB), a transcription factor, as being an important molecule mediating long-term memory formation after spaced training. We also review the main upstream proteins that regulate CREB in different model organisms. Those include the eukaryotic translation initiation factor (eIF2α), protein phosphatase I (PP1), mitogen-activated protein kinase (MAPK), and the protein tyrosine phosphatase corkscrew. Finally, we discuss PKC activation and protein synthesis and degradation as mechanisms by which neurons decode the spacing intervals.

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“…The requirement for a local tag would restrict long-term plasticity to active synapses thereby ensuring appropriate selectivity and specificity. 55,56 This idea was formulated into the synaptic tagging theory, which postulated that even weak stimulation is capable of laying down a local, synaptic tag which renders synapses transiently receptive to long-term synaptic changes via proteins induced by strong stimulation of a different synapse on the same cell. 57 The phenomenon of synaptic tagging was experimentally demonstrated in hippocampal slices where it was found that weak tetanic stimulation that normally leads to only E-LTP can instead induce L-LTP at a synapse if multiple spaced tetani have recently been applied to other input neurons in the same population.…”

Section: Rna Regulation Is Central To Long-term Memory Formationmentioning

confidence: 99%

Long-term memory consolidation: The role of RNA-binding proteins with prion-like domains

Sudhakaran

Ramaswami

2016

RNA Biology

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Long-term and short-term memories differ primarily in the duration of their retention. At a molecular level, long-term memory (LTM) is distinguished from short-term memory (STM) by its requirement for new gene expression. In addition to transcription (nuclear gene expression) the translation of stored mRNAs is necessary for LTM formation. The mechanisms and functions for temporal and spatial regulation of mRNAs required for LTM is a major contemporary problem, of interest from molecular, cell biological, neurobiological and clinical perspectives. This review discusses primary evidence in support for translational regulatory events involved in LTM and a model in which different phases of translation underlie distinct phases of consolidation of memories. However, it focuses largely on mechanisms of memory persistence and the role of prion-like domains in this defining aspect of long-term memory. We consider primary evidence for the concept that Cytoplasmic Polyadenylation Element Binding (CPEB) protein enables the persistence of formed memories by transforming in prion-like manner from a soluble monomeric state to a self-perpetuating and persistent polymeric translationally active state required for maintaining persistent synaptic plasticity. We further discuss prion-like domains prevalent on several other RNA-binding proteins involved in neuronal translational control underlying LTM. Growing evidence indicates that such RNA regulatory proteins are components of mRNP (RiboNucleoProtein) granules. In these proteins, prion-like domains, being intrinsically disordered, could mediate weak transient interactions that allow the assembly of RNP granules, a source of silenced mRNAs whose translation is necessary for LTM. We consider the structural bases for RNA granules formation as well as functions of disordered domains and discuss how these complicate the interpretation of existing experimental data relevant to general mechanisms by which prion-domain containing RBPs function in synapse specific plasticity underlying LTM.

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Discussion

Cited by 39 publications

References 0 publications

Memory Synapses Are Defined by Distinct Molecular Complexes: A Proposal

Memory Synapses Are Defined by Distinct Molecular Complexes: A Proposal

Molecular Determinants of the Spacing Effect

Long-term memory consolidation: The role of RNA-binding proteins with prion-like domains

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