Recent data show that a significant fraction of cortical pyramidal neurons has an axon originating from a basal dendrite (axon-carrying dendrite, AcD) rather than from the soma. In the rodent hippocampus, these AcD cells convey privileged synaptic excitation especially in network states with strong perisomatic inhibition (Hodapp et al., 2022). We have recently shown that hippocampal AcD cells receive stronger commissural input than neurons with somatic axon origin (non-AcD) (Stevens et al., 2023).AcD cells are also present in the neocortex, though seemingly less frequent than in the hippocampus (~20% compared to ~30-50%; Thome et al., 2014, Wahle et al., 2022). However, nothing is known about the network integration of neocortical AcD versus non-AcD cells. We therefore studied commissural inputs in the mouse primary motor cortex (M1), an area with strong interhemispheric connections. Channelrhodopsin 2 was expressed in presynaptic neurons of adult mice by viral injection into the contralateral M1 and whole-cell patch clamp recordings were performed from layer V AcD and non-AcD pyramidal cells in coronal slices of the M1. The vast majority of all recorded cells responded with strong inward currents to optogenetic activation of presynaptic inputs. Repetitive activation of commissural inputs at 20Hz showed prominent paired-pulse depression, without overt differences between both morphological subtypes. Reconstruction of recorded neurons revealed that 16/64 (i.e. 25%) were AcD neurons, while 66 % had a somatic axon origin and 9% a shared axonal/dendritc root. Our data show strong commissural innervation of both, AcD and non-AcD pyramidal neurons in the mouse M1.