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5‐HT stimulates eEF2 dephosphorylation in a rapamycin‐sensitive manner in Aplysia neurites
Author(s) -
Carroll Matthew,
Warren Otis,
Fan Xiaotang,
Sossin Wayne S.
Publication year - 2004
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2004.02634.x
Subject(s) - aplysia , elongation factor , microbiology and biotechnology , eukaryotic translation elongation factor 1 alpha 1 , biology , neurite , phosphorylation , dephosphorylation , kinase , translation (biology) , biochemistry , neuroscience , rna , phosphatase , messenger rna , ribosome , in vitro , gene
In Aplysia , serotonin mediates behavioral sensitization by increasing the strength of the synapse between sensory and motor neurons, a process known as facilitation. The retention of long‐term facilitation is blocked by rapamycin, an inhibitor of a specific translational pathway. One possible rapamycin‐sensitive target is the increased translation of 5′‐terminal oligopyrimidine mRNAs. These transcripts encode components of the translational machinery and have been proposed to be important for retention of long‐term facilitation. We have cloned the 5′‐terminal oligopyrimidine mRNA encoding eukaryotic elongation factor 2 and shown that serotonin increased its translation in synaptosomes. Another possible rapamycin‐sensitive target is the inactivation of eukaryotic elongation factor 2 kinase. Eukaryotic elongation factor 2 kinase phosphorylates and inactivates eukaryotic elongation factor 2, blocking translational elongation. Serotonin application decreased eukaryotic elongation factor 2 phosphorylation in synaptosomes and in isolated neurites, and this was blocked by rapamycin. We propose a role for the rapamycin‐sensitive pathway in neurons. Stimulation blocks translation by inducing calcium entry and phosphorylation of eukaryotic elongation factor 2. This block is reversed through activation of the rapamycin‐sensitive system and dephosphorylation of eukaryotic elongation factor 2.