Defining memories by their distinct molecular traces

Sossin, Wayne S.

doi:10.1016/j.tins.2008.01.001

Cited by 23 publications

(27 citation statements)

References 60 publications

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“…Moreover, the length of time a memory lasts is related to the molecular memory traces formed by the experience (Sossin, 2008). In particular, evidence suggests that production of a constitutively active kinase, known as protein kinase M (PKM), acts as a molecular memory trace.…”

Section: Introductionmentioning

confidence: 99%

Serotonin-Induced Cleavage of the Atypical Protein Kinase C Apl III inAplysia

et al. 2012

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A constitutively active kinase, known as protein kinase M (PKM), is proposed to act as a long-lasting molecular memory trace. While PKM is formed in rodents through translation of a transcript initiating in an intron of the protein kinase C (PKC) gene, this transcript does not exist in Aplysia californica despite the fact that inhibitors of PKM erase memory in Aplysia in a fashion similar to rodents. We have previously shown that, in Aplysia, the ortholog of PKC, PKC Apl III, is cleaved by calpain to form a PKM after overexpression of PKC Apl III. We now show that kinase activity is required for this cleavage. We further use a FRET reporter to measure cleavage of PKC Apl III into PKM Apl III in live neurons using a stimulus that induces plasticity. Our results show that a 10 min application of serotonin induces cleavage of PKC Apl III in motor neuron processes in a calpain-and protein synthesis-dependent manner, but does not induce cleavage of PKC Apl III in sensory neuron processes. Furthermore, a dominant-negative PKM Apl III expressed in the motor neuron blocked the late phase of intermediate-term facilitation in sensory-motor neuron cocultures induced by 10 min of serotonin. In summary, we provide evidence that PKC Apl III is cleaved into PKM Apl III during memory formation, that the requirements for cleavage are the same as the requirements for the plasticity, and that PKM in the motor neuron is required for intermediate-term facilitation.

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Section: Introductionmentioning

confidence: 99%

Serotonin-Induced Cleavage of the Atypical Protein Kinase C Apl III inAplysia

et al. 2012

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“…A similar dynamics of plasma membrane receptor states was suggested by Agnati et al [151], who proposed that the receptor distribution in the plasma membranes of neuronal cells are centered on a few attractors in the state space. Sossin [162] described that longterm memory formation may arise form the repeated inputs of short-term memory stimuli involving de novo protein synthesis, but may also arise as a consequence of a single, strong stimulus involving morphological changes. Song et al [163] examined the long-term facilitation of sensory-motor neuron synapses, and established a protein kinase A-dependent positive feedback loop providing a bistable switch in protein kinase A activity.…”

Section: Network-related Mechanisms Of Learning and Memory Formationmentioning

confidence: 99%

System Level Mechanisms of Adaptation, Learning, Memory Formation and Evolvability: The Role of Chaperone and Other Networks

Gyurko

Sőti

Steták

et al. 2014

CPPS

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During the last decade, network approaches became a powerful tool to describe protein structure and dynamics. Here, we describe first the protein structure networks of molecular chaperones, then characterize chaperone containing sub-networks of interactomes called as chaperone-networks or chaperomes. We review the role of molecular chaperones in short-term adaptation of cellular networks in response to stress, and in long-term adaptation discussing their putative functions in the regulation of evolvability. We provide a general overview of possible network mechanisms of adaptation, learning and memory formation. We propose that changes of network rigidity play a key role in learning and memory formation processes. Flexible network topology provides 'learningcompetent' state. Here, networks may have much less modular boundaries than locally rigid, highly modular networks, where the learnt information has already been consolidated in a memory formation process. Since modular boundaries are efficient filters of information, in the 'learning-competent' state information filtering may be much smaller, than after memory formation. This mechanism restricts high information transfer to the 'learning competent' state. After memory formation, modular boundary-induced segregation and information filtering protect the stored information. The flexible networks of young organisms are generally in a 'learning competent' state. On the contrary, locally rigid networks of old organisms have lost their 'learning competent' state, but store and protect their learnt information efficiently. We anticipate that the above mechanism may operate at the level of both protein-protein interaction and neuronal networks.

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“…It is often stated that STM is consolidated in a protein-synthesis-dependent manner into LTM ((e.g., Davis and Squire, 1984), Sossin, 2008). Alternatively, memories might consist of distinct molecular traces that last for different periods of time; these traces can be graded by their "volatility," traces encoded by activation of protein kinases are more volatile than traces encoded by morphological changes at preexisting synapses (Sossin, 2008;Squire and Davies, 1981).…”

Section: Memories and Molecular Tracesmentioning

confidence: 99%

Section: Memories and Molecular Tracesmentioning

confidence: 99%

“…Alternatively, memories might consist of distinct molecular traces that last for different periods of time; these traces can be graded by their "volatility," traces encoded by activation of protein kinases are more volatile than traces encoded by morphological changes at preexisting synapses (Sossin, 2008;Squire and Davies, 1981). The least volatile ("static") traces are due to the generation and stabilization of new synapses; importantly, whereas at the cellular level these traces are generated independently of each other, they might be linked at the network level where volatile memory traces are required to set up a cellular network that is in turn required to induce the static memory trace (Sossin, 2008). Sweatt (2009) see also Telese et al, 2013 describes recent discoveries demonstrating that experience can drive the production of epigenetic marks in the adult nervous system and that the experience-dependent regulation of epigenetic (mechanisms that allow a heritable change in gene expression in the absence of DNA mutation; Rahn et al, 2013;Roopra et al, 2012) molecular mechanisms in the mature central nervous system participates in the control of gene transcription underlying the formation of LTMs.…”

Section: Memories and Molecular Tracesmentioning

confidence: 99%

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