Neocortical pyramidal cells with axon-carrying basal dendrites: a prominent feature regulated by activity

Abstract

Axon-carrying dendrites, AcDs, have been reported in hippocampus to be privileged dendrites which can directly feed synaptic inputs into an axonal output bypassing the soma and escaping somatic inhibition. In non-primate neocortex, 15–20% of the pyramidal cells have basal AcDs and comparable proportions occurred in organotypic cortex cultures. How does an axon happen to emerge from a dendrite? Very immature migrating pyramidal neurons have no basal dendrites but already have an axon. Sprouts were seen to emerge from the very proximal portion of axons suggesting that an AcD cell starts out as a ‘dendrite-carrying axon’ (DcA) cell. Further, the formation of basal AcD was influenced by neuronal activity. Inhibition of GluN2B receptors, overexpression of strongly calcium binding indicator proteins and activity deprivation impaired basal dendritic growth and reduced the proportion of AcD pyramidal neurons. In contrast, perinatal enhancement of glutamatergic network activity with kainate or carbachol via subplate neurons accelerated the appearance of AcD pyramidal neurons. None of the treatments altered the proportion of AcD interneurons. Together, the larvae stage of a cortical AcD pyramidal neuron can well be the DcA configuration, and the formation of basal AcDs was - at least transiently – regulated by neuronal activity, calcium and glutamatergic signaling.