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Serotonergic innervation of the prefrontal cortex (PFC) modulates neuronal activity and PFC functions. However, the cellular mechanism for serotonergic modulation of neuronal excitability remains unclear. We performed patch-clamp recording at the axon of layer-5 pyramidal neurons in rodent PFC slices. We found surprisingly that the activation of 5-HT 1A  receptors selectively inhibits Na +  currents obtained at the axon initial segment (AIS) but not those at the axon trunk. In addition, Na +  channel subtype Na V 1.2 but not Na V 1.6 at the AIS is selectively modulated by 5-HT 1A  receptors. Further experiments revealed that the inhibitory effect is attributable to a depolarizing shift of the activation curve and a facilitation of slow inactivation of AIS Na +  currents. Consistently, dual somatic and axonal recording and simulation results demonstrate that the activation of 5-HT 1A  receptors could decrease the success rate of action potential (AP) backpropagation toward the somatodendritic compartments, enhancing the segregation of axonal and dendritic activities. Together, our results reveal a selective modulation of Na V 1.2 distributed at the proximal AIS region and AP backpropagation by 5-HT 1A  receptors, suggesting a potential mechanism for serotonergic regulation of functional polarization in the dendro-axonal axis, synaptic plasticity and PFC functions.

Selective Modulation of Axonal Sodium Channel Subtypes by 5-HT 1A Receptor in Cortical Pyramidal Neuron