Cortical degeneration in the absence of neurotrophin signaling: Dendritic retraction and neuronal loss after removal of the receptor TrkB

To examine functions of TrkB in the adult CNS, TrkB has been removed from n eurons expressing CaMKII, primarily pyramidal neurons, using Cre-mediated r ecombination. A floxed trkB allele was designed so that neurons lacking Trk B express tau-beta-galactosidase. Following trkB deletion in pyramidal cell s, their dendritic arbors are altered, and cortical layers II/III and V are compressed, after which there is an apparent loss of mutant neurons expres sing the transcription factor SCIP but not of those expressing Otx-1. Loss of neurons expressing SCIP requires deletion of trkB within affected neuron s; reduction of neuronal ER81 expression does not, suggesting both direct a nd indirect effects of TrkB loss. Thus, TrkB is required for the maintenanc e of specific populations of cells in the adult neocortex.