Mind bomb-1 is an essential modulator of long-term memory and synaptic plasticity via the Notch signaling pathway

Mol Brain. 2012 Oct 30:5:40. doi: 10.1186/1756-6606-5-40.

Abstract

Background: Notch signaling is well recognized as a key regulator of the neuronal fate during embryonic development, but its function in the adult brain is still largely unknown. Mind bomb-1 (Mib1) is an essential positive regulator in the Notch pathway, acting non-autonomously in the signal-sending cells. Therefore, genetic ablation of Mib1 in mature neuron would give valuable insight to understand the cell-to-cell interaction between neurons via Notch signaling for their proper function.

Results: Here we show that the inactivation of Mib1 in mature neurons in forebrain results in impaired hippocampal dependent spatial memory and contextual fear memory. Consistently, hippocampal slices from Mib1-deficient mice show impaired late-phase, but not early-phase, long-term potentiation and long-term depression without change in basal synaptic transmission at SC-CA1 synapses.

Conclusions: These data suggest that Mib1-mediated Notch signaling is essential for long-lasting synaptic plasticity and memory formation in the rodent hippocampus.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / metabolism
  • Animals
  • Hippocampus / anatomy & histology
  • Hippocampus / enzymology
  • Long-Term Potentiation
  • Memory, Long-Term / physiology*
  • Mice
  • Mice, Knockout
  • Neuronal Plasticity / physiology*
  • Neurons / metabolism
  • Phenotype
  • Protein Kinase C / metabolism
  • Protein Structure, Tertiary
  • Receptors, Notch / chemistry
  • Receptors, Notch / metabolism*
  • Signal Transduction*
  • Synapses / physiology*
  • Ubiquitin-Protein Ligases / metabolism*

Substances

  • Receptors, Notch
  • MIB1 protein, mouse
  • Ubiquitin-Protein Ligases
  • protein kinase C zeta
  • Protein Kinase C