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This Article Full Text Full Text (PDF) All Versions of this Article: 102/3/1443    most recent 00287.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Gorini, C. Articles by Mendelowitz, D. PubMed PubMed Citation Articles by Gorini, C. Articles by Mendelowitz, D.

Serotonergic Modulation of the Trigeminocardiac Reflex Neurotransmission to Cardiac Vagal Neurons in the Nucleus Ambiguus

Department of Pharmacology and Physiology, The George Washington University, Washington, DC

Submitted 31 March 2009; accepted in final form 16 June 2009

Abstract

Stimulation of the trigeminal nerve evokes a dramatic decrease in heart rate and blood pressure, and this reflex has generally been termed the trigeminocardiac reflex. A subset of the trigeminocardiac reflex is the diving reflex in which the nasal mucosa is stimulated with water or air-borne chemical irritants. Activation of the diving reflex evokes a pronounced bradycardia, mediated by increased parasympathetic cardiac activity, and is the most powerful autonomic reflex. However, exaggeration of this protective response could be detrimental and has been implicated in Sudden Infant Death Syndrome (SIDS). Despite the importance and strength of the trigeminocardiac reflex, there is little information about the cellular mechanisms and brain stem pathways that constitute this reflex. To address these issues, stimulation of trigeminal afferent fibers and the evoked excitatory postsynaptic currents were recorded in cardiac vagal neurons (CVNs) in an in vitro brain stem slice preparation. This synaptic pathway is robust and activation of the trigeminal pathway often evoked action potentials in CVNs. Application of the serotonin (5-HT) reuptake inhibitor citalopram significantly enhanced these responses. Consistent with the hypothesis this pathway is endogenously modulated by 5-HT receptors the 5-HT_1A receptor antagonist, WAY 100635 inhibited, whereas the 5-HT_2A/C receptor antagonist, ketanserin facilitated the excitatory neurotransmission to CVNs. The 5-HT_1A receptor agonist 8-hydroxy-2-(dipropylamino)tetralin hydrobromide increased, whereas the 5-HT₂ receptor agonist, -methylserotonin maleate salt inhibited this reflex pathway. These results indicate stimulation of trigeminal fibers evokes a powerful excitatory and polysynaptic pathway to CVNs, and this pathway is endogenously modulated and differentially enhanced and depressed, by 5-HT_1A and 5-HT₂ receptors, respectively.