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5HT1A Receptor Mediated Inhibition of Glutamatergic Neurotransmission to Cardiac Vagal Neurons Following Hypoxia and Hypercapnia
Author(s) -
Mendelowitz David,
Kamendi Harriet W
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1009.2
Subject(s) - glutamatergic , serotonergic , neurotransmission , purinergic receptor , excitatory postsynaptic potential , neuroscience , hypercapnia , chemistry , receptor , endocrinology , medicine , inhibitory postsynaptic potential , biology , serotonin , glutamate receptor , acidosis
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.