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Plasticity product : ウィキペディア英語版
Plasticity product

Plasticity Product is a term coined by Jerry Rudy to refer to mRNA genetic artifacts and protein products triggered by transcription factors leading to long-lasting long term potentiation.〔Rudy, J. (2008). The neurobiology of learning and memory. Sunderland Mass.: Sinauer Associates Inc. Publishers.〕
==Introduction==
The term "plasticity product" was coined by Jerry Rudy to refer to mRNA genetic artifacts and protein products triggered by transcription factors, leading long-lasting long term potentiation (L-LTP) and sustained alterations in synaptic strength.〔
Rudy differentiates between two types of long term potentiation: S-LTP (short-lasting) and L-LTP (long-lasting). In S-LTP the stimulus is strong enough to induce long-term potentiation but too weak to trigger intracellular events necessary to sustain synaptic changes. L-LTP is much less transient than S-LTP and involves the generation of new proteins through translation and transcription.〔
Induction of L-LTP depends on the transcription of new mRNA and the translation of these new mRNA into proteins. These steps are encompassed by the genomic signaling hypothesis as follows:〔
:#A stimulus is strong enough to induce L-LTP is delivered.
:#A signaling cascade begins, leading to phosphorylation of transcription factors.
:#mRNA is produced leading to subsequent translation of new proteins to sustain synaptic changes.
Support for the genomic signaling hypothesis comes from studies conducted by Nguyen et al. demonstrating the inability to induce L-LTP following transcription inhibition immediately following the inducing stimulus but not if transcription is blocked later. The temporal effects of this inhibition suggests that L-LTP is dependent on newly synthesized "plasticity products."〔Nguyen, P., Abel, T., & Kandel, E. (1994). Requirement of a critical period of transcription for induction of a late phase of LTP. ''Science'', 265(5175), 1104-1107. 〕
cAMP-responsive element-binding (CREB) protein, a transcription factor, is also implicated in changes in synaptic plasticity. Inhibition of CREB translation likewise inhibited synaptic changes. CREB is activated in its phosphorylated form, acting as a molecular switch for production of plasticity products.〔Dash, P. K., Hochner, B., & Kandel, E. R. (1990). Injection of the cAMP-responsive element into the nucleus of Aplysia sensory neurons blocks long-term facilitation. ''Nature'', 345(6277), 718-721. 〕

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