Prenatal Nicotinic Exposure (PNE) Prolongs Superior Laryngeal C‐Fibers (SLCFs)‐mediated Apnea through Upregulating TRPV1 Receptor

Abstract

Maternal cigarette smoke is a critical factor in the pathogenesis of sudden infant death syndrome (SIDS). Simulation of SLCFs evokes an immediate apnea and cardiovascular instability, which are potentially life‐threatening and implicated in pathogenesis of SIDS. To date, the impact of PNE on SLCFs has not been explored. We tested hypothesis whether PNE could prolong the SLCF‐mediated apnea, and if so, whether this prolongation is associated with an upregulated expression of TRPV1 on nodose/jugular (N/J) ganglionic neurons retrogradely traced from the superior laryngeal nerve (SLN). To this end, we compared following outcomes between Ctrl and PNE rat pups (postnatal days 11–14): 1) the apneic response to intralaryngeal application of capsaicin (10 μg/kg, 50 μl) to stimulate local TRPV1 in anesthetized preparation; 2) immunoreactivity of TRPV1 in laryngeal sensory neurons of N/J ganglia retrogradely traced by DiI; and 3) TRPV1 currents recorded by whole‐cell patch clamp on cultured sensory laryngeal C‐neurons from N/J ganglia retrogradely traced by DiI. Our results showed that PNE: 1) markedly prolonged the SLCF‐mediated apnea; 2) significantly increased the expression TRPV1 receptors in N/J ganglionic C‐neurons; and 3) augmented the amplitudes of TRPV1 currents on these neurons. The results suggest that PNE is able to prolong the SLCF‐mediated apnea likely though upregulating TRPV1 receptor expression, which may contribute to SIDS.Support or Funding InformationSupported by HL‐107462 and HL‐119683