5HT1A receptors inhibit glutamate inputs to cardiac vagal neurons post-hypoxia/hypercapnia

► 5HT1A receptors do not alter excitatory neurotransmission to cardiac vagal neurons (CVNs) under control conditions. ► During recovery from Hypoxia/Hypercapnia an endogenous serotonergic pathway inhibits glutamatergic transmission to CVNs. ► A decrease in 5-HT1A activation would augment glutamate input to CVNs causing bradycardia in diseases such as SIDS and OSA.