Impaired hippocampal long-term potentiation in microtubule-associated protein 1B-deficient mice

Mark Zervas, Thoralf Opitz, Winfried Edelmann, Bruce Wainer, Raju Kucherlapati, Patric K. Stanton

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


Microtubule-associated protein (MAP)1B-heterozygous (MAP1B+/-) mice are deficient in the expression of MAP1B in the hippocampus, cerebellum, and olfactory cortex. Although MAP1B+/- mice showed half the normal levels of MAP1B protein, they had no measurable amounts of phosphorylated MAP1B. High-frequency θ burst stimulation of Schaffer collateral-CA1 axons in hippocampal slices from MAP1B+/- mice elicited long-term potentiation (LTP) that decayed rapidly to baseline, in contrast to the non-decremental LTP exhibited by age-matched wild-type slices. A separate group of MAP1B+/- and wild-type slices was examined for a longer time course of 3 hr post-tetanus in response to multiple high-frequency stimulus trains that induced saturated LTP. MAP1B+/-slices showed marked reductions in both immediate post-tetanic potentiation and LTP that decayed much more rapidly than that in wild-type slices. The induction of LTP was associated with a rapid dephosphorylation of MAP1B within 5-15 min post-tetanus, suggesting that the normal expression of MAP1B and conversion to a dephosphorylated state may be a cellular mediator of cytoskeletal alterations necessary for long-term activity-dependent synaptic plasticity.

Original languageEnglish (US)
Pages (from-to)83-92
Number of pages10
JournalJournal of Neuroscience Research
Issue number1
StatePublished - Oct 1 2005


  • CA1
  • Cytoskeleton
  • Dendrite
  • Hippocampus
  • LTP
  • MAP1B
  • Mouse
  • Synaptic plasticity

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience


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