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J Neurosci. 2011 Jun 15;31(24):8841-50. doi: 10.1523/JNEUROSCI.1358-11.2011.

Persistent long-term synaptic plasticity requires activation of a new signaling pathway by additional stimuli.

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  • 1Department of Neuroscience, Columbia University College of Physicians and Surgeons, New York State Psychiatric Institute, New York, New York 10032, USA. jh2004@columbia.edu

Abstract

Most memories are strengthened by additional stimuli, but it is unclear how additional stimulation or training reinforces long-term memory. To address this we examined whether long-term facilitation (LTF) of Aplysia sensorimotor synapses in cell culture-a cellular correlate of long-term sensitization of defensive withdrawal reflexes in Aplysia californica-can be prolonged by additional stimulation. We found that 1 d treatment with serotonin (5-HT; five brief applications at 20 min intervals) produced LTF lasting ∼3 d, whereas 2 d of such 5-HT treatments induced a persistent LTF lasting >7 d. Incubation with the protein synthesis inhibitor rapamycin during the second set of 5-HT treatments abolished all facilitation, and synapse strength returned prematurely to baseline. Persistent LTF required more persistent elevation in the expression of the neurotrophin-like peptide sensorin and its secretion. Activation of protein kinase C (PKC) during the second day of 5-HT treatments, not required for LTF or changes in sensorin expression during the first set of 5-HT treatments, is critical for persistent LTF and replaces phosphoinositide 3 kinase (PI3K) activity in mediating the increase in sensorin expression. In contrast, activations of PKC during the first day of 5-HT treatments and PI3K during the second day of 5-HT treatments are unnecessary for persistent LTF or the increases in sensorin expression. Thus, additional stimuli make preexisting plasticity labile as they recruit a new signaling cascade to regulate the synthesis of a neurotrophin-like peptide required for persistent alterations in synaptic efficacy.

PMID:
21677168
[PubMed - indexed for MEDLINE]
PMCID:
PMC3152308
Free PMC Article
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