| Title | Serotonergic Modulation of the Trigeminocardiac Reflex Neurotransmission to Cardiac Vagal Neurons in the Nucleus Ambiguus. | | Author(s) | Gorini CJ, Jameson HS, Mendelowitz D | | Institution | George Washington University. | | Source | J Neurophysiol 2009 Jun 24. | | 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 brainstem pathways that constitute this reflex. To address these issues stimulation of trigeminal afferent fibers and the evoked excitatory post-synaptic currents (EPSCs) were recorded in cardiac vagal neurons (CVNs) in an in-vitro brainstem 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-HT1A receptor antagonist, WAY 100635 inhibited, whereas the 5-HT2A/C receptor antagonist, ketanserin facilitated the excitatory neurotransmission to CVNs. The 5-HT1A receptor agonist DPAT increased, whereas the 5-HT2 receptor agonist, alpha-methyl-5-HT 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-HT1A and 5-HT2 receptors, respectively. | | Language | ENG | | Pub Type(s) | JOURNAL ARTICLE
| | PubMed ID | 19553488 |
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