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Biochemical Pathways by Which Serotonin Regulates Translation in the Nervous System of Aplysia
Author(s) -
Yanow Stephanie K.,
Manseau Frédéric,
Hislop Jonathan,
Castellucci Vincent F.,
Sossin Wayne S.
Publication year - 1998
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 - 10.1046/j.1471-4159.1998.70020572.x
Subject(s) - aplysia , protein biosynthesis , biology , protein kinase a , translation (biology) , microbiology and biotechnology , synaptic plasticity , translational regulation , messenger rna , protein kinase c , cgmp dependent protein kinase , kinase , biochemistry , mitogen activated protein kinase kinase , neuroscience , receptor , gene
In the marine mollusk Aplysia californica , serotonin initiates three phases of translational regulation: an initial decrease in translation, followed by a transient increase in protein synthesis, both of which are independent of transcription, followed by a later increase in protein synthesis that is dependent on transcription. These increases in protein synthesis may underlie translation‐dependent changes in synaptic plasticity. We have characterized the second messenger pathways that underlie these changes in the pleural ganglia of Aplysia . Activation of protein kinase C was both necessary and sufficient for the initial decrease in translation. Protein kinase C, cyclic AMP‐dependent protein kinase, and a tyrosine kinase were all required for the second phase, a transient increase in protein synthesis. The late increase in protein synthesis required both protein kinase A and spaced applications of serotonin. Rapamycin, a specific inhibitor of a downstream translational regulator, blocked the transient increase in protein synthesis (second phase), suggesting that this drug may be useful in determining the specific physiological consequences of this translational regulation. Indeed, we used rapamycin to demonstrate that one type of intermediate form of synaptic plasticity induced by serotonin did not require the rapamycin‐sensitive increase in translation.