Journal
NEURON
Volume 61, Issue 1, Pages 113-125Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2008.10.049
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Funding
- NIH [2R01MH041083-19]
- NSF [IOB-0444762j]
- W.M. Keck Foundation
- NRSA [5F31MH70065-2]
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An activity-dependent form of intermediate memory (AD-ITM) for sensitization is induced in Aplysia by a single tail shock that gives rise to plastic changes (AD-ITF) in tail sensory neurons (SNs) via the interaction of action potential firing in the SN coupled with the release of serotonin in the CNS. Activity-dependent long-term facilitation (AD-LTF, lasting > 24hr) requires protein synthesis dependent persistent mitogen-activated protein kinase (MAPK) activation and translocation to the SN nucleus. We now show that the induction of the earlier temporal phase (AD-ITM and AD-ITF), which is translation and transcription independent, requires the activation of a compartmentally distinct novel signaling cascade that links second messengers, MAPK and PKC into a unified pathway within tail SNs. Since both AD-ITM and AD-LTM require MAPK activity, these collective findings suggest that presynaptic SNs route e flow of molecular information to distinct subcellular compartments during the induction of activity-dependent long-lasting memories.
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