Mice deficient in microtubule-associated protein MAP1B show a distinct behavioral phenotype and altered retina function.

We investigated mice deficient for the microtubule-associated protein MAP1B, a cytoskeletal element highly expressed in the developing nervous system, for altered performance in behavior, learning, and memory. Using the multiple T-maze, the open field and the Morris water maze we found that mice homozygous for a deletion of the MAP1B gene demonstrate impaired locomotor activity most likely correlated to a lack of physical endurance in general. In contrast, there were no significant differences in cognitive function and memory retention. In addition, we performed electroretinography and observed a reduction of the a-wave amplitude in response to single flash, white light stimulation. Taken together, these data provide further evidence for an important role of MAP1B in synaptic neurotransmission.