title: [Effects of Methyleugenol on central respiratory drive to inspiratory-activated airway vagal preganglionic neurons].
abstract: OBJECTIVE
  To explore the effects of methyleugenol (MEG) on central respiratory drive to inspiratory-activated airway vagal preganglionic neurons (IA-AVPNs).
  
  
  METHODS
  The 3 to 5-day-old Sprague-Dawley rats were anesthetized and rhodamine was injected into trachea wall for labelling IA-AVPNs in ventrolateral vicinity of nucleus ambiguous (vNA). And then a brainstem slice preparation with hypoglossal rootlets was made. IA-AVPNs were identified and excitatory synaptic inputs were recorded with patch-clamp techniques. Brainstem slice preparations were divided into the groups of control prior to application of MEG and MEG during MEG application. The data from the last 10 consecutive inspiratory phases prior to application of MEG were chosen as control. And the data from the last 5 respiratory cycles prior to rhythm blockade were used to represent the maximal effects of MEG group. Paired Student's t-test was used for comparing inter-group differences.
  
  
  RESULTS
  Compared with control, MEG group had lower frequency, amplitude, duration and area of hypoglossal bursts (2.14 ± 0.87 vs 5.39 ± 1.93 burst/min, 1.27 ± 0.53 vs 2.94 ± 0.92 mV, 178 ± 37 vs 249 ± 54 ms, 330 ± 173 vs 983 ± 534 mV · ms, all P < 0.001). The duration, amplitude and area of phasic inspiratory inward current were lower in MEG group, accounting for (66.3 ± 4.4)%, (58.5 ± 4.3)%, (44.9 ± 7.5)% (all P < 0.05) of control respectively. Compared with control, the frequency of phasic excitatory postsynaptic currents (EPSCs) was lower (29.87 ± 3.70 vs 42.27 ± 11.95 Hz) during inspiratory bursts but the amplitude was higher (83.13 ± 15.97 vs 49.26 ± 7.40 pA) (all P < 0.05). However, compared with control, no significant differences existed in the frequency and amplitude of tonic EPSCs during inspiratory intervals (all P > 0.05).
  
  
  CONCLUSIONS
  MEG inhibits central respiratory drive to IA-AVPNs through inhibiting excitatory synaptic transmission.
authors.affiliation: Department of Respiratory Medicine, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai 200080, China.
authors.forename: Lili
authors.initials: L
authors.lastname: Hou
authors.affiliation: Department of Respiratory Medicine, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai 200080, China; Email: xzhou53@163.com.
authors.forename: Xin
authors.initials: X
authors.lastname: Zhou
authors.affiliation: Department of Respiratory Medicine, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai 200080, China.
authors.forename: Min
authors.initials: M
authors.lastname: Zhang
authors.affiliation: Department of Respiratory Medicine, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai 200080, China.
authors.forename: Zhenwei
authors.initials: Z
authors.lastname: Liu
authors.affiliation: Department of Respiratory Medicine, Shanghai First People's Hospital, Shanghai Jiaotong University, Shanghai 200080, China.
authors.forename: Guoqing
authors.initials: G
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001933:Brain Stem; D005054:Eugenol / Q000031:analogs & derivatives; D019706:Excitatory Postsynaptic Potentials; D008526:Medulla Oblongata; D009474:Neurons; D018408:Patch-Clamp Techniques; D051381:Rats; D017207:Rats, Sprague-Dawley; D012137:Respiratory System; D014630:Vagus Nerve
chemical_list: C005223:methyleugenol; D005054:Eugenol