ArticleLearning & memory (Cold Spring Harbor, N.Y.)
Role of Aplysia cell adhesion molecules during 5-HT-induced long-term functional and structural changes.
Article in Learning & memory (Cold Spring Harbor, N.Y.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Structural Components of Synaptic Plasticity and Memory Consolidation.Cold Spring Harbor perspectives in biology · 2015Review
- Learning-related synaptic growth mediated by internalization of Aplysia cell adhesion molecule is controlled by membrane phosphatidylinositol 4,5-bisphosphate synthetic pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Mapping molecular memory: navigating the cellular pathways of learning.Cellular and molecular neurobiology · 2012Review
- The molecular and cellular biology of enhanced cognition.Nature reviews. Neuroscience · 2009Review
- Transcriptome analysis and identification of regulators for long-term plasticity in Aplysia kurodai.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Transcriptional regulation of long-term memory in the marine snail Aplysia.Molecular brain · 2008Review
- PKA-activated ApAF-ApC/EBP heterodimer is a key downstream effector of ApCREB and is necessary and sufficient for the consolidation of long-term facilitation.The Journal of cell biology · 2006Article
- BDNF mobilizes synaptic vesicles and enhances synapse formation by disrupting cadherin-beta-catenin interactions.The Journal of cell biology · 2006Article
- Cofilin expression induces cofilin-actin rod formation and disrupts synaptic structure and function in Aplysia synapses.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that five repeated pulses of 5-HT lead to down-regulation of the TM-apCAM isoform at the surface of Aplysia sensory neurons (SNs). We here examined whether apCAM down-regulation is required for 5-HT-induced long-term facilitation. We also analyzed the role of the cytoplasmic and extracellular domains by overexpressing various apCAM mutants by DNA microinjection. When TM-apCAM was up-regulated in SNs by DNA microinjection, five pulses of 5-HT failed to produce either synaptic facilitation or an enhancement of synaptic growth, suggesting that down-regulation of apCAM is required for 5-HT-induced EPSP enhancement and new varicosity formation. However, disrupting the extracellular domain function of overexpressed apCAM with a specific antibody restored 5-HT-induced excitatory postsynaptic potential increase but not synaptic growth. The overexpression of the MAP Kinase mutant of TM-apCAM, which is not internalized by 5-HT, inhibited new varicosity formation, but did not inhibit excitatory postsynaptic potential increase. Deletion mutants containing only the cytoplasmic portion of apCAM blocked 5-HT-induced synaptic growth but not excitatory postsynaptic potential increase. Thus, our data suggest that TM-apCAM may act as a suppressor of both synaptic-strength enhancement in pre-existing synapses and of new synaptic varicosity formation in the nonsynaptic region, via different mechanisms.
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