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Activation of the diving reflex and excitation of cardiac vagal neurons (CVNs) in the nucleus ambiguus (NA)
Author(s) -
Gorini Christopher,
Mendelowitz David
Publication year - 2007
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.21.5.a471
Subject(s) - reflex , nucleus ambiguus , excitatory postsynaptic potential , brainstem , stimulation , neuroscience , vagovagal reflex , trigeminal nerve , medicine , vagus nerve , anesthesia , bradycardia , reflex bradycardia , anatomy , heart rate , biology , medulla oblongata , central nervous system , receptor , blood pressure
The diving reflex is the most powerful autonomic reflex. Stimulation of the diving reflex by activation of nasotrigeminal sensory fibers evokes a pronounced bradycardia, mediated by increased parasympathetic cardiac activity in both humans and other mammals. The diving reflex is highly pronounced in man with heart rate decreasing in the range from 5–51% upon a single facial submersion. In this study we examined the excitation of CVNs upon stimulation of the trigeminal nerve to evoke the diving reflex. In an initial surgery, Sprague‐Dawley rats (postnatal days 2–7) were anesthetized and received a right thoractomy. The retrograde tracer rhodamine was injected onto the terminals of CVNs in the fat pads at the base of the heart to label CVNs. On the day of the experiments (2–4 days later), CVNs in the NA were identified in brainstem slices by the fluorescent tracer and studied using the whole‐cell patch‐clamp technique. Stimulation of the trigeminal nerve evoked a powerful excitatory neurotransmission to CVNs. This excitatory input occurred with a latency of 20–30 msec and was blocked by focal application of the glutamatergic antagonists AP5 and CNQX. Application of the muscarinic agonist bethanechol inhibited this excitatory pathway. These results provide a foundation for understanding the transmitters and receptors that mediate and modulate the brainstem pathways that constitute the diving reflex.