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

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 theta 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.

journal_name

J Neurosci Res

authors

Zervas M,Opitz T,Edelmann W,Wainer B,Kucherlapati R,Stanton PK

doi

10.1002/jnr.20624

keywords:

subject

Has Abstract

pub_date

2005-10-01 00:00:00

pages

83-92

issue

1

eissn

0360-4012

issn

1097-4547

journal_volume

82

pub_type

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