{'fraction_non_alphanumeric': 0.021145975443383355, 'fraction_numerical': 0.01296043656207367, 'mean_word_length': 5.216101694915254, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Ketamine alters the trigeminal cardiac brainstem reflex pathway

The trigemino‐cardiac reflex (TCR) can be evoked by activating the trigeminal nerve and induces bradycardia, hypotension and apnea. Although it is known that the central circuit for the TCR is intrinsic to the brainstem, the brainstem circuitry, receptors and mechanisms responsible for this reflex are unknown. The goals of this study are to identify the synaptic connections involved in the TCR pathway and the effect of anesthetics ketamine, isoflurane, and fentanyl on the synaptic responses in trigeminal neurons and cardiac vagal neurons (CVNs) upon stimulation of the trigeminal nerve rootlet. A retrograde viral vector was used to identify trigeminal sensory fibers in prenatal rats in vitro. Stimulation of trigeminal afferent fibers evoked an EPSC in brainstem trigeminal neurons. The average latency of the initial evoked EPSC was 1.86 ± 0.3 ms, suggesting this afferent pathway is a monosynaptic event. The non‐NMDA receptor antagonist, CNQX completely blocked the response. Electric stimulation of trigeminal nerve also induced polysynaptic excitatory currents in CVNs. The average latency of the evoked sEPSC in CVNs was 12.1 ± 1.1 ms. The peak amplitude of sEPSC was inhibited by ketamine but enhanced by fentanyl. These findings suggest that ketamine and fentanyl differentially alter the synaptic pathways that constitute the TCR. The research is supported by AHA grant 10BGIA3720042.