To examine functions of TrkB in the adult CNS, TrkB has been removed from neurons expressing CaMKII, primarily pyramidal neurons, using Cre-mediated recombination. A floxed trkB allele was designed so that neurons lacking TrkB express tau-β-galactosidase. Following trkB deletion in pyramidal cells, their dendritic arbors are altered, and cortical layers II/III and V are compressed, after which there is an apparent loss of mutant neurons expressing the transcription factor SCIP but not of those expressing Otx-1. Loss of neurons expressing SCIP requires deletion of trkB within affected neurons; reduction of neuronal ER81 expression does not, suggesting both direct and indirect effects of TrkB loss. Thus, TrkB is required for the maintenance of specific populations of cells in the adult neocortex.
Bibliographical noteFunding Information:
We thank Dr. William Mobley for comments on the manuscript and Sheri Harris for help in blind analyses of neuronal counts. We thank Dr. Greg Lemke for antibodies to SCIP and Drs. Silvia Arber and Thomas Jessell for antibodies to ER81. We thank Drs. Liliana Minichiello and Rüdiger Klein for sharing results prior to publication. This work has been supported by the Howard Hughes Medical Institute and the National Institute of Neurological Disorders, and Stroke grant P01-16033.