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

✍ Scribed by Mark Zervas; Thoralf Opitz; Winfried Edelmann; Bruce Wainer; Raju Kucherlapati; Patric K. Stanton

Publisher: John Wiley and Sons
Year: 2005
Tongue: English
Weight: 347 KB
Volume: 82
Category: Article
ISSN: 0360-4012
DOI: 10.1002/jnr.20624

No coin nor oath required. For personal study only.

✦ Synopsis

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 u 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 wildtype 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 posttetanic 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 activitydependent synaptic plasticity. V

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