Goller F, Larsen O N
Center for Sound Communication, Odense University, Denmark.
J Exp Biol. 1997 Aug;200(Pt 16):2165-76. doi: 10.1242/jeb.200.16.2165.
The in situ biomechanics of the vocal organ, the syrinx, was studied in anesthetized pigeons using fiberoptic instruments. The role of syringeal muscles was determined by electrical stimulation, and phonation was induced by injecting gas into the subsyringeal air sacs. This study presents the first direct observations of the biomechanical processes that occur in an intact syrinx. Contraction of one of the syringeal muscles, the m. tracheolateralis (TL), withdraws the lateral tympaniform membranes (LTM) from the syringeal lumen, causing opening of the syringeal airways. Shortening of a second muscle, the sternotrachealis (ST), draws the syringeal cartilages closer to each other, causing the LTM to fold into the syringeal lumen. Maximal ST contraction does not lead to complete closure of the syrinx. As air-sac pressure is increased by the injection of gas, the LTM are drawn into the syringeal lumen and balloon in a rostral direction until they touch, thus forming a fold-like valve. Air-induced phonation is always associated with vibrations of the membrane folds, suggesting that pulsatile release of air into the trachea by vibratory motion of the LTM generates sound. During air-induced phonation, strong stimulation of the TL terminates sound generation by abducting the LTM, whereas weak stimulation changes the geometry of the membrane folds, which is accompanied by changes in the acoustic structure of the sound. Stimulation of the ST has little effect on air-induced sounds. The LTM appear to be the main sound generators, since disabling the medial tympaniform membranes (MTM) with tissue adhesive does not prevent phonation or change the frequency and amplitude structure of display coos in spontaneously vocalizing pigeons. Moreover, the activity of the syringeal muscles appears to have a mainly modulatory function, suggesting that the basic sound-generating mechanism is similar in both air-induced and natural phonation.
利用光纤仪器在麻醉的鸽子身上研究了发声器官鸣管的原位生物力学。通过电刺激确定鸣管肌肉的作用，并通过向鸣管下方气囊注入气体诱导发声。本研究首次直接观察了完整鸣管中发生的生物力学过程。鸣管肌肉之一气管外侧肌（TL）收缩，使外侧鼓室膜（LTM）从鸣管腔中缩回，导致鸣管气道开放。另一块肌肉胸骨气管肌（ST）缩短，使鸣管软骨彼此靠近，导致LTM折叠进入鸣管腔。ST最大收缩不会导致鸣管完全关闭。随着注入气体使气囊压力增加，LTM被吸入鸣管腔并向头侧膨胀，直到它们接触，从而形成褶皱状瓣膜。空气诱导发声总是与膜褶皱的振动相关，这表明LTM的振动运动使空气脉冲式释放到气管中产生声音。在空气诱导发声期间，强烈刺激TL会通过使LTM外展而终止声音产生，而弱刺激会改变膜褶皱的几何形状，这伴随着声音声学结构的变化。刺激ST对空气诱导的声音影响很小。LTM似乎是主要的声音发生器，因为用组织粘合剂使内侧鼓室膜（MTM）失能并不会阻止发声，也不会改变自发发声鸽子展示咕咕声的频率和振幅结构。此外，鸣管肌肉的活动似乎主要具有调节功能，这表明在空气诱导发声和自然发声中基本的声音产生机制是相似的。
