Structural alterations of spiny stellate cells in the somatosensory cortex in ephrin-A5-deficient mice.

Previous studies demonstrated that in ephrin-A5-deficient mice corticothalamic arbors are reduced by more than 50% in layer 4 of the somatosensory cortex (S1), where ephrin-A5 is normally expressed. Here we examined possible consequences of the reduced thalamic input on spiny stellate cells, the target neurons of thalamocortical afferents. Using ballistic delivery of particles coated with lipophilic dyes in fixed slices and confocal laser-microscopy, we could quantitatively analyze the morphology of these neurons. Cells were examined in S1 at postnatal day 8 (P8), when thalamic afferents establish synaptic contacts and the dendrites of their target cells are covered with filopodia, and at P23, after synapse formation and replacement of filopodia by spines. Our results indicate that at P8 the dendrites of cells in mutant animals exhibit more filopodia and are more branched than dendrites of wildtype cells. In contrast, there is no difference in the extent of the dendritic tree between knockout and control animals. At P23, dendrites of neurons in ephrin-A5-deficient mice are still more branched, but possess fewer spines than wildtype cells. Thus, at early stages layer 4 neurons appear to compensate the reduced thalamic input by increasing dendritic branching and the density of filopodia. However, while at later stages the dendrites of layer 4 neurons in mutants are still more branched, their spine density is now lower than in wildtype cells. Taken together, these data demonstrate that the structure of spiny stellate cells is shaped by thalamic input and Eph receptor signaling.