5HT1A Receptor Mediated Inhibition of Glutamatergic Neurotransmission to Cardiac Vagal Neurons Following Hypoxia and Hypercapnia

Abstract

Cardiac vagal neurons (CVNs) are excited by serotonergic and purinergic pathways recruited post hypoxia / hypercapnia (H/H). Surprisingly, excitatory glutamatergic inputs to CVNs are inhibited post H/H. This study examines the mechanisms of H/H induced inhibition of glutamatergic neurotransmission to CVNs. Spontaneous and inspiratory‐related EPSCs were recorded from identified CVNs before, during and post H/H. WAY 100635 (100 microM), a specific antagonist for 5HT1A receptors, restored a glutamatergic pathway to CVNs in the recovery period following H/H. The purinergic and serotonergic pathways to CVNs active post H/H were not altered by blocking 5HT1A receptors and WAY 100635 had no effect before, and during H/H. This study indicates endogenous activation of serotonergic 5HT1A receptors decreases glutamatergic neurotransmission to CVNs following H/H, likely via a presynaptic site of action.