A nucleolar protein ApLLP induces ApC/EBP expression required for long-term synaptic facilitation in aplysia neurons

Neuron. 2006 Mar 2;49(5):707-18. doi: 10.1016/j.neuron.2006.01.035.

Abstract

In Aplysia, long-term synaptic plasticity is induced by serotonin (5-HT) or neural activity and requires gene expression. Here, we demonstrate that ApLLP, a novel nucleolus protein, is critically involved in both long-term facilitation (LTF) and behavioral sensitization. Membrane depolarization induced ApLLP expression, which activated ApC/EBP expression through a direct binding to CRE. LTF was produced by a single pulse of 5-HT 30 min after the membrane depolarization. This LTF was blocked when either ApLLP or ApC/EBP were blocked by specific antibodies. In contrast, ApLLP overexpression induced LTF in response to a single 5-HT treatment. Simultaneously, a siphon noxious stimulus (SNS) to intact Aplysia induced ApLLP and ApC/EBP expression, and single tail shock 30 min after SNS transformed short-term sensitization to long-term sensitization of siphon withdrawal reflex. These results suggest that ApLLP is an activity-dependent transcriptional activator that switches short-term facilitation to long-term facilitation.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Aplysia / cytology*
  • Avoidance Learning / physiology
  • Behavior, Animal
  • Blotting, Western / methods
  • CCAAT-Enhancer-Binding Proteins
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Electric Stimulation / methods
  • Electrophoretic Mobility Shift Assay / methods
  • Gene Expression / drug effects
  • Gene Expression / physiology*
  • Gene Expression Regulation / physiology*
  • Gene Expression Regulation / radiation effects
  • Green Fluorescent Proteins / metabolism
  • Immunohistochemistry / methods
  • In Situ Hybridization / methods
  • Long-Term Potentiation / drug effects
  • Long-Term Potentiation / physiology*
  • Long-Term Potentiation / radiation effects
  • Microinjections / methods
  • Models, Biological
  • Neurons / classification
  • Neurons / cytology
  • Neurons / drug effects
  • Neurons / metabolism*
  • Potassium / pharmacology
  • Promoter Regions, Genetic / physiology
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction / methods
  • Serotonin / pharmacology
  • Time Factors
  • Transcription Factors / metabolism*
  • Transcriptional Activation

Substances

  • CCAAT-Enhancer-Binding Proteins
  • RNA, Messenger
  • Transcription Factors
  • Green Fluorescent Proteins
  • Serotonin
  • Potassium