Developmental Changes in Potassium Channels in Low Threshold Myelinated Ah-type Vagal Ganglion Neurons in Rats

•Ah-type VGNs decline at 4 weeks days old which closed to adulthood in males.•The development changes of K+ currents contribute to the sexual dimorphism of Ah-types.•Ah-type VGNs might transform to A-type VGNs in males along with age. Myelinated Ah-type vagal ganglion neurons (VGNs) were specific subpopulation in adult females, rather than neonate and key players in sexual dimorphism in baroreflex afferent function and closely associated with estrogen. However, the gender related development changes in Ah-type VGNs remains unknown. To quantify the developmental changes in ion channels overtime, the whole-cell patch-clamp technique was performed and three afferent fiber types of VGNs were identified upon electrophysiological/pharmacological validations. The K+ currents were recorded with or without specific blockers from postnatal day 4–32 and adult in both sexes. The electrophysiological data conjugated with analysis of action potential (AP) trajectory strongly indicated that in male rats, Ah-types were likely to disappear or transform during development. The percentage of myelinated A-, Ah-, and unmyelinated C-type afferents in females remained relatively steady during the 4–32-day period. Conversely, Ah-type afferents in males declined from levels comparable with those in females at birth to near absence in adulthood at 32 days. The coordinated changes in the current density of certain ion channels may be the underlying mechanism of developmental changes in AP waveform and neuroexcitability. As expected, the coordinated change between the down-regulation of iberiotoxin-sensitive and up-regulation of 4-aminopyridine-sensitive K+ currents played a key role in shaping AP and neuroexcitability in Ah-types during development. Our results demonstrated that the myelinated Ah-type VGNs in males almost disappear at 4 weeks old where closes to adult and the correlative ion channel changes contribute to the sexual dimorphism in visceral afferent function.