Laryngeal Activity Research Articles

Tuning phenomena of melodies and resonance frequencies (formants) in infants pre-speech utterances

In a former study [Wermke et al., Med. Eng. Phys. 24, 501–514 (2002)], an increasing tuning between laryngeal (melody) and pharyngeal (resonance frequencies) activity was demonstrated during pre-speech development. This tuning was observed unexpectedly early during development in mitigated cries and earliest non-cry utterances and prepares probably articulation in speech-like vocalizations of older infants. A new retrospective study supported this assumption by comparing tuning processes in cries and early non-cry utterances (N=2500) in two groups (low versus high word production performance at 18 months) of term-born healthy infants (N=20). Additionally, age-matched comparisons were made in 4 cleft-lip-palate-infants treated with a palatal plate. In order to demonstrate the interaction between melody and resonance control we designed a special graphical representation. The tracking function of the resonance frequencies is displayed synchronously to the melody and its harmonics. Resonance frequencies in pre-speech utterances are not yet identical to formant bands associated with speech sounds. The results support the existence of an early active tuning and its relation to later speech. This behavior seems to prepare formant tuning in later speech. Medical applications are seen for infants with disturbances of the vocal tract transfer function, e.g., infants with cleft-lip-palate. [Work supported by DFG.]

Phonetic study of North American languages history and results

Serious phonetic study of North America languages started at the beginning of the 20th century. Within limits of available technology, aspects of speech articulation, aerodynamics and acoustics were investigated. One clear motivation was to understand how classes of sounds unfamiliar from study of better-known European and Asian languages were produced. Glottalized consonants and stops then referred to as ‘‘intermediate’’ (voiceless unaspirated) received particular attention. Nasal airflow, lip position in vowels, and tone and pitch accent were also investigated. Significant insights on relative timing were obtained, inter alia foreshadowing VOT measurement as a useful discriminator of laryngeal activity and revealing part of the mechanism by which ejective consonants are made. After the 1920’s, the idea of ‘‘psychologically real’’ phonemes which ignored phonetic differences became the ruling paradigm in American linguistics, contributing to a decline of interest in phonetic studies that basically lasted until around the 1980’s. When interest renewed, a new vision that phonetic patterns show regularities independent of phonemic structure guided research, and considerable attention was also paid to how indigenous American languages fit into overall phonetic typologies. Recent work is also often informed by concern for documentation of endangered languages and community interest in language revival.

Arterial pulse modulated activity is expressed in respiratory neural output

Although it is well-established that sympathetic activity is modulated with respiration, it is unknown whether neural control of respiration is reciprocally influenced by cardiovascular function. Even though previous studies have suggested the existence of pulse modulation in respiratory neurons, they could not exclude the possibility that such cells were involved in cardiovascular rather than respiratory motor control, owing to neuroanatomic and functional overlaps between brain stem neurons involved in respiratory and cardiovascular control. The aim of this study was to test the hypothesis that respiratory motoneurons and putative premotoneurons are modulated by arterial pulse. An existing data set composed of 72 well-characterized, respiratory-modulated brain stem motoneurons and putative premotoneurons was analyzed using delta(2), a recently described statistic that quantifies the magnitude of arterial pulse-modulated spike activity [Dick TE and Morris KF. J Physiol 556: 959-970, 2004]. Neuronal activity was recorded in the rostral and caudal ventral respiratory groups of 19 decerebrate, neuromuscular-blocked, ventilated cats. Axonal projections were identified by rectified and unrectified spike-triggered averages of recurrent laryngeal nerve activity or by antidromic activation from spinal stimulation electrodes. The firing rates of approximately 30% of these neurons were modulated in phase with both the respiratory and cardiac cycles. Furthermore, arterial pulse modulation occurred preferentially in the expiratory phase in that only expiratory neurons had high delta(2) values and only expiratory activity had significant delta(2) values after partitioning tonic activity into the inspiratory and expiratory phases. The results demonstrate that both respiratory motoneurons and putative premotoneuronal activity can be pulse modulated. We conclude that a cardiac cycle-related modulation is expressed in respiratory motor activity, complementing the long-recognized respiratory modulation of sympathetic nerve activity.

Cough and laryngeal muscle discharges in brainstem lesioned anaesthetized cats.

Experiments were carried out to determine whether there are separate drives from the selected neuronal networks of the brainstem affecting the discharge patterns of laryngeal and respiratory pump muscles during cough. Twenty-four non-decerebrate spontaneously breathing cats anesthetized with sodium pentobarbitone were used. Microinjections of kainic acid into the lateral tegmental field of the medulla, medullary midline or pontine respiratory group eliminated the cough evoked by mechanical stimulation of the tracheobronchial and laryngopharyngeal mucosa. These stimuli, in most cases, provoked irregular bursts of discharges in the posterior cricoarytenoid and thyroarytenoid laryngeal muscles (or they had no effect on them). No pattern of laryngeal muscle activities following lesions resembled the laryngeal cough response. Lesions of the target regions did not result in any apparent changes in the eupnoeic pattern of laryngeal activity. Neurons of the medullary lateral tegmental field, raphe nuclei and the pontine respiratory group seem to be indispensable for the configuration of the central cough motor pattern. However, these neurons do not appear to be essential for the discharge patterns of laryngeal motoneurons during eupnoea. The residual laryngeal "cough" responses are probably mediated by an additional motor drive.

Monosynaptic circuitry of trigeminal proprioceptive afferents coordinating jaw movement with visceral and laryngeal activities in rats

Jaw movement is intimately related to various oromotor and visceral functions such as feeding, swallowing, vocalization, respiration and cardiac function. Neuronal circuitry that links jaw movement and these visceral and oromotor functions is largely unknown. The purpose of this study is to determine whether the trigeminal proprioceptive and jaw-muscle spindle afferents send axons to and synapse with the motoneurons innervating visceral organs and laryngeal muscles utilizing multiple double-labeling and physiological approaches. Double labeling of anterograde tracing combined to retrograde transport was performed by injection of biotinylated dextran amine into the mesencephalic trigeminal nucleus and cholera toxin B subunit or horseradish peroxidase into the vagus nerve and the recurrent laryngeal nerve. Mesencephalic trigeminal nucleus neuronal terminals contacted with visceral and laryngeal muscle motoneurons in the ambiguus nucleus and the nearby intermediate reticular zone. By electron microscopic observation, we confirmed that mesencephalic trigeminal nucleus terminals made asymmetric axodendritic synapses with these motoneurons. Double labeling of physiologically characterized jaw muscle spindle afferent neurons combined with anti-choline acetyltransferase immunohistochemistry showed that jaw-muscle spindle afferent boutons closely contacted choline acetyltransferase-immunoreactive motoneurons in the ambiguus nucleus and intermediate reticular zone. This report is the first to demonstrate that the trigeminal proprioceptive afferents synapsed upon visceral and laryngeal muscle motoneurons and provide neuronal networks for the jaw–visceral and jaw–laryngeal coordination.

Laryngeal Electromyographic, Cardiovascular, and Respiratory Effects of Neuropeptide Injections into the Nucleus Tractus Solitarius of Rats

Identifying central neurotransmitters that mediate laryngeal adductor activity may aid in managing pathological laryngeal adduction as occurs in laryngospasm or apparent life-threatening events in infants. We studied the effect on cricothyroid (CT) and thyroarytenoid (TA) electromyography (EMG) and on cardiovascular parameters of neurotransmitter injections into the rat nucleus tractus solitarius (NTS), the primary sensory relay center of the larynx. Twenty nanoliters of vasoactive intestinal peptide (VIP; 2.5 pmol), neurokinin B (NKB, 16 pmol), calcitonin gene-related peptide (3.0 pmol), neurokinin A (NKA; 35 pmol), or artificial cerebrospinal fluid (control solution) was stereotactically injected into the region of the NTS and the control nucleus gracilis in 119 studies performed in 24 mature, anesthetized Sprague-Dawley rats. Changes in diaphragm, CT, and TA EMG activity and blood pressure (BP) were compared. Injection sites were verified histologically. Injections of both VIP and NKB into the region of the NTS, but not the nucleus gracilis, induced life-threatening changes, including apnea, a marked decline in BP (p < .05), and increases in EMG activity of the CT and TA adductor muscles ranging from sustained contraction to mild phasic increases during inspiration. Calcitonin gene-related peptide injection also decreased BP (p < .05), but caused only mild increases in CT and TA EMG activity. NKA and control injections into the NTS did not alter respiration, BP, or CT or TA EMG activity. VIP and NKB may play important roles in modulating EMG activity of the CT and TA muscles. This information may prove useful in evaluating pharmacological targets of central reflex activity to manage life-threatening laryngeal adduction.

Nonnutritive swallowing and respiration relationships in preterm lambs.

The aim of the present study was to assess the effects of the different states of alertness on 1) nonnutritive swallowing (NNS) frequency, 2) the relationship between NNS and the respiratory cycle, and 3) the association of NNS with spontaneous apneas. Recordings of sleep states, diaphragm and laryngeal constrictor electrical activity, nasal flow, electrocardiogram, respiratory inductance plethysmography, and pulse oximetry were obtained from six preterm lambs without sedation. Analysis of 2,468 NNS showed that 1) NNS frequency was higher during quiet wakefulness and active sleep (AS) than in quiet sleep; 2) in all states of alertness, a greater number of NNS (38%) were preceded and followed by an inspiration; 3) although NNS and central apneas were rarely coincidental, AS appeared to favor their association; and 4) most obstructive apneas occurred in AS and were coincidental with bursts of NNS. Compared with results in full-term lambs, premature birth does not modify the NNS-respiratory coordination. However, AS in preterm lambs is characterized by a higher association of NNS bursts with obstructive apneas.

Producing VOT contrasts

The development of voice onset time (VOT) as an acoustic index for studying and classifying stop consonants also prompted a large number of studies examining laryngeal activity and interarticulator timing related to VOT. A collaboration between the Research Institute of Logopedics and Phoniatrics at the University of Tokyo and Haskins Laboratories resulted in a long line of studies using electromyographic and other techniques that provided much of the empirical foundations for what we know about laryngeal function in speech, in particular the production of voiced and voiceless consonants. This presentation will review the articulatory control of VOT differences. To make a consonant voiceless, a speaker uses a combination of glottal abduction and vocal fold tensing. The distinction between voiceless stops with long and short VOT is basically due to a difference in the timing between the glottal abduction gesture and the oral closing and opening gestures. Variations in the size of the glottal gesture also occur. More generally, variations in interarticulator timing between glottal and oral movements are used to produce the different stop categories that occur in the languages of the world. [Work supported by NIH.]

Preoptic hypothalamic warming suppresses laryngeal dilator activity during sleep.

Upper airway dilator activity during sleep appears to be diminished under conditions of enhanced sleep propensity, such as after sleep deprivation, leading to worsening of obstructive sleep apnea (OSA). Non-rapid eye movement (NREM) sleep propensity originates in sleep-active neurons of the preoptic area (POA) of the hypothalamus and is facilitated by activation of POA warm-sensitive neurons (WSNs). We hypothesized that activation of WSNs by local POA warming would inhibit activity of the posterior cricoarytenoid (PCA) muscle, an airway dilator, during NREM sleep. In chronically prepared unrestrained cats, the PCA exhibited inspiratory bursts in approximate synchrony with inspiratory diaphragmatic activity during waking, NREM, and REM. Integrated inspiratory PCA activity (IA), peak activity (PA), and the lead time (LT) of the onset of inspiratory activity in PCA relative to diaphragm were significantly reduced in NREM sleep and further reduced during REM sleep compared with waking. Mild bilateral local POA warming (0.5-1.2 degrees C) significantly reduced IA, PA, and LT during NREM sleep compared with a prewarming NREM baseline. In some animals, effects of POA warming on PCA activity were found during waking or REM. Because POA WSN activity is increased during spontaneous NREM sleep and regulates sleep propensity, we hypothesize that this activation contributes to reduction of airway dilator activity in patients with OSA.

The regulation of respiratory resistance in exercising horses.

Horses display remarkable aerobic capabilities, attaining during muscular exercise a maximal rate of oxygen consumption about 30-fold higher than the resting value, and 2.5-fold higher than that of other mammals of similar body mass. Under these circumstances an enormous mechanical burden is expected to impinge on the equine respiratory pump and regulatory mechanisms aiming to minimize this load may play an important role in determining the adequacy of the respiratory system to the metabolic requirements. The behaviour of the respiratory system has been investigated in horses at rest and during treadmill locomotion at different velocities and gaits. During exercise hyperpnoea, horses exhibit a significant reduction in the lung viscous resistance not observed in other mammals, such as dogs and humans. Therefore, the exercise-dependent increase in the rate of mechanical work of breathing is lower in the horse than in other mammals. This increase in the equine airway patency during exercise appeared to be mainly determined by the pattern of laryngeal movements. In fact, during exercise, the laryngeal cross-sectional area, determined with a video-endoscopic imaging technique at the level of rima glottidis (CSArg), undergoes during inspiration an increase averaging up to over 4 times the resting expiratory values. Although a significant linear correlation was found between CSArg and minute ventilation (VE), the laryngeal activation contributes to increase lung conductance only when CSArg is narrower than the tracheal section. It appears therefore that in exercising horses pulmonary resistive features are finely controlled to reduce the mechanical load supported by the respiratory muscles and to counterbalance the increase in the ventilatory energetic requirements inherent in the remarkably enhanced aerobic performance observed in this species.

The neuronal circuit of augmenting effects on intrinsic laryngeal muscle activities induced by nasal air-jet stimulation in decerebrate cats

We previously demonstrated that during nasal air-jet stimulation, both the activities of intrinsic laryngeal adductor and abductor muscles persistently increase, whereas the respiratory cycle prolongs and the activity of diaphragm decreases [Am. J. Rhinol. 9 (1995) 203–208; Neurosci. Res. 31 (1998) 137–146]. The purpose of this study was to clarify the neuronal circuit underlying the augmentation of intrinsic laryngeal muscles evoked by nasal air-jet stimulation. The immunohistologic analysis of Fos-expression was reported to determine the distribution of activated neurons in cat brainstem evoked by sneeze-inducing air puff stimulation of the nasal mucosa [Brain Res. 687 (1995) 143–154]. In sneezing cats, immunoreactivity was evoked in projection areas of the ethmoidal afferents, e.g. the subnuclei caudalis, interpolaris and in interstitial islands of the trigeminal sensory complex. Immunoreactivity was also enhanced in the solitary complex, the nucleus retroambiguus, the pontine parabrachial area and the lateral aspect of the parvocellular reticular formation [Brain Res. 687 (1995) 143–154]. In the present study, we focussed on the parvocellular reticular nucleus (PRN) as a relay of the neural circuit contributed to the augmentation of intrinsic laryngeal muscles evoked by nasal air-jet stimulation. We recorded the neuronal behavior of PRN during the nasal air-jet stimulation in precollicular-postmammillary decerebrate cats. As the results, 24% (17/71) of recorded neurons which were activated orthodromically by the electrical stimulation to anterior ethmoidal nerve, increased their firing rates in response to the nasal air-jet stimulation. Furthermore, spike-triggered averaging method revealed that four of these 17 PRN neurons activated intrinsic laryngeal muscles, suggesting that such neurons have excitatory projections to the intrinsic laryngeal muscle motoneurons in the nucleus ambiguus. These results suggest that the some of PRN neuron play a role in augmentation of the intrinsic laryngeal muscles activities during nasal air-jet stimulation.

Emergence of oropharyngeal, laryngeal and swallowing activity in the developing fetal upper aerodigestive tract: an ultrasound evaluation.

The developing fetal upper aerodigestive system provides the structural support for respiratory and ingestive functions necessary to sustain life at birth. This study investigated prenatal development of upper aerodigestive anatomy and the association of emerging functions as predictors of postnatal feeding skills. Biometric measures of oral, lingual, pharyngeal and laryngeal structures were obtained in fetuses 15-38 weeks gestational age using a four-plane sonographic technique. Accompanying ingestive behaviors were tallied across development. The data from 62 healthy controls were compared to seven cases at risk for postnatal feeding and swallowing dysfunction (Type II Arnold Chiari Malformation, trisomy 18, polyhydramnios, intrauterine growth restriction, Brachmann-de Lange Syndrome). Significant (p<0.001) linear regressions occurred in pharyngeal and lingual growth across gestation while ingestive behavior such as suckling emerged in a sequence of basic to complex movement patterns. Jaw and lip movements progressed from simple mouth opening to repetitive open-close movements important for postnatal suckling. Lingual movements increased in complexity from simple forward thrusting and cupping to anterior-posterior motions necessary for successful suckling at term. Laryngeal movements varied from shallow flutter-like movements along the lumen to more complex and complete adduction-abduction patterns. Fetal swallowing primarily occurred in the presence of concomitant oral-facial stimulatory activity. Significant variations (p<0.01) in the form and function of the ingestive system occurred in comparisons of gestational age-matched controls to at-risk cases. We postulate that prenatal developmental indices of emerging aerodigestive skills may guide postnatal decisions for feeding readiness and, ultimately, advance the care of the premature, medically fragile neonate.

Glycinergic inhibition is essential for co-ordinating cranial and spinal respiratory motor outputs in the neonatal rat.

Eupnoeic breathing in mammals is dependent on the co-ordinated activity of cranial and spinal motor outputs to both ventilate the lungs and adjust respiratory airflow, which they do by regulating upper-airway resistance. We investigated the role of central glycinergic inhibition in the co-ordination of cranial and spinal respiratory motor outflows. We developed an arterially perfused neonatal rat preparation (postnatal age 0-4 days) to assess the effects of blocking glycine receptors with systemically administered strychnine (0.5-1 microM). We recorded respiratory neurones located within the ventrolateral medulla, inspiratory phrenic nerve activity (PNA) and recurrent laryngeal nerve activity (RLNA), as well as dynamic changes in laryngeal resistance. Central recordings of postinspiratory neurones revealed an earlier onset in firing relative to the onset of inspiratory PNA after exposure to strychnine (260 +/- 38.9 vs. 129 +/- 26.8 ms). After glycine receptor blockade, postinspiratory neurones discharged during the inspiratory phase. Strychnine also evoked a decrease in PNA frequency (from 38.6 +/- 4.7 to 30.7 +/- 2.8 bursts min(-1)), but amplitude was unaffected. In control conditions, RLNA comprised inspiratory and postinspiratory discharges; the amplitude of the latter exceeded that of the former. However, after administration of strychnine, the amplitude of inspiratory-related discharge increased (+65.2 +/- 15.2 %) and exceeded postinspiratory activity. Functionally this change in RLNA caused a paradoxical, inspiratory-related glottal constriction during PNA. We conclude that during the first days of life in the rat, glycine receptors are essential for the formation of the eupnoeic-like breathing pattern as defined by the co-ordinated activity of cranial and spinal motor inspiratory and postinspiratory activities.

Mechanisms of airway protection during retching, vomiting, and swallowing.

We investigated the mechanisms of airway protection and bolus transport during retching and vomiting by recording responses of the pharyngeal, laryngeal, and hyoid muscles and comparing them with responses during swallowing and responses of the gastrointestinal tract. Five dogs were chronically instrumented with electrodes on the striated muscles and strain gauges on smooth muscles. Retching and vomiting were stimulated by apomorphine (5-10 ug/kg iv). During retching, the hyoid and thyroid descending and laryngeal abductor muscles were activated; between retches, the hyoid, thyroid, and pharyngeal elevating, and laryngeal adductor muscles were activated. Vomiting always occurred during the ascending phase of retching and consisted of three sequential phases of hyoid and pharyngeal muscle activation culminating in simultaneous activation of all recorded elevating and descending laryngeal, hyoid, and pharyngeal muscles. Retrograde activation of esophagus and pharyngeal muscles occurred during the later phases, and laryngeal adductor was maximally activated in all phases of the vomit. During swallowing, the laryngeal adductor activation was followed immediately by brief activation of the laryngeal abductor. We concluded that retching functions to mix gastric contents with refluxed intestinal secretions and to impart an orad momentum to the bolus before vomiting. During retches, the airway is protected by glottal closure, and between retches, it is protected by ascent of the larynx and closure of the upper esophageal sphincter. The airway is protected by maximum glottal closure during vomiting. During swallowing, the airway is protected by laryngeal elevation and glottal closure followed by brief opening of the glottis, which may release subglottal pressure expelling material from the laryngeal vestibule.

Effect of upper airway negative pressure and lung inflation on laryngeal motor unit activity in rabbit.

Distortion of the upper airway by negative transmural pressure (UANP) causes reflex vagal bradycardia. This requires activation of cardiac vagal preganglionic neurons, which exhibit postinspiratory (PI) discharge. We hypothesized that UANP would also stimulate cranial respiratory motoneurons with PI activity. We recorded 32 respiratory modulated motor units from the recurrent laryngeal nerve of seven decerebrate paralyzed rabbits and recorded their responses to UANP and to withholding lung inflation using a phrenic-triggered ventilator. The phasic inspiratory (n = 17) and PI (n = 5) neurons detected were stimulated by -10 cmH(2)O UANP and by withdrawal of lung inflation (P < 0.05, Friedman's ANOVA). Expiratory-inspiratory units (n = 10) were tonically active but transiently inhibited in postinspiration; this inhibition was more pronounced and prolonged during UANP stimuli and during no-inflation tests (P < 0.05). We conclude that, in addition to increasing inspiratory activity in the recurrent laryngeal nerve, UANP also stimulates units with PI activity.

Effects of carbonic anhydrase inhibition on the responsiveness of laryngeal receptors in cats to CO2.

The effects of carbonic anhydrase inhibition on the responsiveness to CO2 of pressure-sensitive laryngeal receptors were examined in anaesthetised, paralysed cats. Laryngeal CO2-sensitive receptors from the superior laryngeal nerve were selected by their responsiveness to intralaryngeal pressure and to perfusion of solution equilibrated with 9% CO2. The carbonic anhydrase inhibitor, methazolamide, when given intralaryngeally at 10(-4) M, diminished or abolished the responses to the CO2-equilibrated solution in four of six pressure-sensitive receptors. Histochemical staining for carbonic anhydrase activity showed that the larynges perfused with methazolamide had diminished carbonic anhydrase activity, especially on the superficial layers of surface epithelium. Compared to untreated controls, when given intravenously (50 mg x kg(-1)) methazolamide diminished or abolished the responses to CO2 of five of the six fibres studied. Histochemical staining of these larynges showed no carbonic anhydrase reactivity at the sites of laryngeal receptors. These results suggest that the responses to CO2 of laryngeal pressure-sensitive receptors are dependent on the presence of carbonic anhydrase. Inhibition of laryngeal receptor carbonic anhydrase activity by methazolamide is more reliably achieved by systemic rather than by luminal administration.

Internal superior laryngeal nerve afferent activity during respiration and evoked vocalization in cats.

The purpose of this project was to identify and categorize patterns of activity of the internal branch of the superior laryngeal nerve during vocalization evoked by midbrain stimulation in cats anesthetized with alpha-chloralose. Unit activity was isolated from the cut distal end of the internal branch of the superior laryngeal nerve by means of floating bipolar electrodes that retained their contact with nerve fibers despite movement due to vocalization. The phases of respiration and vocalization were determined with a diaphragm electromyogram, a photoglottogram, and a microphone recording. Five groups of discrete afferent activities were defined according to relationships between the spike activity and the phases of vocalization. Group 1 cell activity peaked just before phonation, during expiratory airflow (n = 26). Group 2 cells (n = 19) followed a vocal fold vibratory pattern during phonation. Group 3 cell activity (n = 6) peaked during phonation, but did not follow vocal fold vibration. Group 4 cells (n = 3) were active during inspiration between phonations. Group 5 cells (n = 4) showed both inspiratory and expiratory modulation. These results indicate that laryngeal afferent activity responds to phonation-specific events during vocalization. This stereotyped afferent information might be used by the central nervous system to modulate vocalization.

Medullary respiratory neurones and control of laryngeal motoneurones during fictive eupnoea and cough in the cat.

1. This study addressed the hypothesis that ventrolateral medullary respiratory neurones participate in the control of laryngeal motoneurones during both eupnoea and coughing. 2. Data were obtained from 28 mid-collicular decerebrated, artificially ventilated cats. Cough-like motor patterns (fictive cough) in phrenic, lumbar and recurrent laryngeal nerves were elicited by mechanical stimulation of the intrathoracic trachea. Microelectrode arrays were used to monitor simultaneously several neurones in the ventral respiratory group, including the Bötzinger and pre-Bötzinger complexes. Spike trains were evaluated for responses during fictive cough and evidence of functional connectivity with spike-triggered averages of efferent recurrent laryngeal nerve activity. 3. Primary features were observed in averages triggered by 94 of 332 (28 %) neurones. An offset biphasic wave with a positive time lag was present in the unrectified average for 10 inspiratory and 13 expiratory neurones. These trigger neurones were respectively identified as inspiratory laryngeal motoneurones with augmenting, decrementing, plateau and "other" discharge patterns, and expiratory laryngeal motoneurones with decrementing firing patterns. 4. Rectified averages triggered by inspiratory neurones included 37 offset peaks, 11 central peaks and one offset trough. Averages triggered by expiratory neurones had 12 offset peaks, six central peaks and four offset troughs. Relationships inferred from these features included premotor actions of inspiratory neurones with augmenting, decrementing, plateau and "other" patterns on inspiratory laryngeal motoneurones, and premotor actions of decrementing and "other" expiratory neurones on expiratory laryngeal motoneurones. Corresponding changes in neuronal firing patterns during fictive cough supported these inferences. 5. The data confirm and extend previous results on the control of laryngeal motoneurones during eupnoea and support the hypothesis that the same premotor neurones help to shape motoneurone firing patterns during both eupnoea and coughing.

Some non-sequential phenomena in German function words

Labellers of connected speech corpora encounter a number of cases which are difficult to handle with a linear sequence of segmental labels. Based on material from a corpus of German unscripted speech, this paper presents non-sequential aspects of laryngeal activity for /x/ and /h/, and of supralaryngeal articulation in vocoid exponents of postvocalic /r/. Comparative data for /r/ from a corpus of German read speech indicate that differences across speaking styles may be independent of durational variation. It is discussed how models of the phonology-phonetics interface and Prosodic Analysis can account for the findings.

Central mechanisms controlling upper airway patency

The neurones of the ponto-medullary respiratory network drive two functionally and anatomically distinct pools of motoneurones. One set is located within the spinal cord that innervates the diaphragm and intercostal muscles. A second group of motoneurones is located within the nucleus ambiguus imbedded in the ventral respiratory group that project via cranial motor outflows to co-ordinate the activity of laryngeal and bronchial muscles to control airway resistance and airflow. These spinal and cranial motor activities have to be precisely co-ordinated to ensure efficient ventilation. We recently included this behaviour as imperative for a definition of eupnoea. Thus, beside a rhythmic eupnoeic (ramp) discharge pattern of pump motoneurones, a phasic respiratory modulation of glottal resistance should be observed and expressed as glottal dilation during inspiration and transient glottal constriction during post-inspiration [1]. During the last decade mechanisms underlying respiratory rhythm generation were studied primarily in reduced in vitro preparations. The work concluded that the respiratory rhythm is generated by pacemaker neurones located in the Pre-Botzinger complex and is independent of inhibitory glycinergic synaptic transmission (for review see [2,3]). However, a potential role for glycinergic transmission for the eupneic co-ordination of circuitry controlling the upper airway was largely disregarded. To determine a role for glycinergic inhibition within the pon-tomedullary network, we used the arterially perfused working heart-brainstem preparation (WHBP) of neonatal and mature rat. This preparation allows both kinesiological and cellular studies of central and peripheral mechanisms controlling upper airway resistance [1]. Recording of the recurrent laryngeal nerve activity as an index of motor output to the glottis revealed post-inspiratory activity that shifted towards the inspiratory phase after strychnine antagonism of glycine receptors (0.5–1.5 μM). This shift of post-inspiratory activity was also obtained at the cellular level: intracellular recordings of post-inspiratory neurones revealed that the hyperpo-larisation during the inspiratory phase was converted to a depolarisation with spike discharge after exposure to strychnine. This lead to a massive disturbance of the eupnoeic modulation of glottal resistance by converting the inspiratory glottic dilatation (seen during control) to a paradoxical constriction, as demonstrated by measuring changes in laryngeal resistance. Similar results were obtained in both neonatal and juvenile rats suggesting that glycinergic mechanisms co-ordinating ventilatory movements with upper airway resistance are functional at birth. The effects of glycinergic inhibition were mimicked during exposure of neonatal preparations to prolonged hypoxia. During the secondary hypoxic depression of respiration post-inspiratory activity was shifted towards inspiration causing a paradoxical glottic constriction during neural inspiration. We conclude that integrity of glycinergic neurotransmission within the ponto-medullary respiratory network is essential for co-ordinating the neuronal activities which control upper airway resistance and ventilatory movements and consequently the eupnoeic breathing pattern in rats from birth.