Abstract
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 language | English (US) |
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Pages (from-to) | 83-92 |
Number of pages | 10 |
Journal | Journal of Neuroscience Research |
Volume | 82 |
Issue number | 1 |
DOIs | |
State | Published - Oct 1 2005 |
Keywords
- CA1
- Cytoskeleton
- Dendrite
- Hippocampus
- LTP
- MAP1B
- Mouse
- Synaptic plasticity
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience