title: Beta-asarone inhibits synaptic inputs to airway preganglionic parasympathetic motoneurons.
abstract: Therapeutic application of Asarum, a herbal medicine that has been used for centuries, reportedly causes acute respiratory disturbance. The responsible constituents, the sites of action, and the mechanisms involved in this side effect are unclear. We investigated the effects of β-asarone, a volatile constituent of Asarum, on neurotransmission in the medullary respiratory neuronal network using extracellular recording of the rhythmic hypoglossal activity and voltage clamp recordings of the postsynaptic activity of the airway preganglionic parasympathetic motoneurons (APPMs) in vitro. β-Asarone caused progressive decreases in the duration and area of the hypoglossal bursts in a concentration-dependent manner. The frequency and amplitude of the bursts were initially unaltered or temporarily increased, but were then inhibited progressively after prolonged exposure. As with the inhibition of the hypoglossal bursts, the tonic and the phasic excitatory and inhibitory postsynaptic currents in the APPMs were attenuated. These data suggest that the Asarum-caused acute respiratory disturbance involves β-asarone-induced inhibition of neurotransmission in the medullary respiratory neuronal network.
authors.affiliation: The State Key Laboratory of Medical Neurobiology and Institute of Brain Sciences, Fudan University Shanghai Medical College, 138 Yi-Xue-Yuan Road, Shanghai 200032, China.
authors.forename: Dongying
authors.initials: D
authors.lastname: Qiu
authors.forename: Lili
authors.initials: L
authors.lastname: Hou
authors.forename: Yonghua
authors.initials: Y
authors.lastname: Chen
authors.forename: Xujiao
authors.initials: X
authors.lastname: Zhou
authors.forename: Wenjun
authors.initials: W
authors.lastname: Yuan
authors.forename: Weifang
authors.initials: W
authors.lastname: Rong
authors.forename: Lei
authors.initials: L
authors.lastname: Zhu
authors.forename: Jijiang
authors.initials: J
authors.lastname: Wang
mesh_terms: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione / Q000494:pharmacology; D000081248:Allylbenzene Derivatives; D000818:Animals; D000840:Anisoles / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005071:Evoked Potentials / Q000187:drug effects; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005343:Fibrinolytic Agents / Q000494:pharmacology*; D018756:GABA Antagonists / Q000494:pharmacology; D005726:Ganglia, Parasympathetic / Q000166:cytology*; D018684:Glycine Agents / Q000494:pharmacology; D007002:Hypoglossal Nerve / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D009046:Motor Neurons / Q000187:drug effects*; D009433:Neural Inhibition / Q000187:drug effects*; D018408:Patch-Clamp Techniques / Q000379:methods; D010852:Picrotoxin / Q000494:pharmacology; D051381:Rats; D012125:Respiratory Center / Q000166:cytology / Q000187:drug effects; D012235:Rhodamines / Q000378:metabolism; D013331:Strychnine / Q000494:pharmacology; D055366:Synaptic Potentials / Q000187:drug effects*; D013997:Time Factors
chemical_list: D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D000081248:Allylbenzene Derivatives; D000840:Anisoles; D018691:Excitatory Amino Acid Antagonists; D005343:Fibrinolytic Agents; D018756:GABA Antagonists; D018684:Glycine Agents; D010852:Picrotoxin; D012235:Rhodamines; D013331:Strychnine; C012195:asarone